Key Points
- 1.
The postanesthesia care unit (PACU) is a specialized unit designed to monitor for early postanesthesia and surgical adverse events.
- 2.
Early cardiac decline after noncardiac surgery requires prompt evaluation, early intervention, and cardiologist consultation for advanced care.
- 3.
Neurohormonal changes and sympathetic nervous system activation can impair cardiac function in patients with cardiac disease.
- 4.
Anesthetic management can be used to suppress adverse effects related to surgical trauma.
- 5.
Fluid resuscitation, medication administration, and underlying comorbidity are areas of consideration for the source of respiratory distress in PACU patients.
- 6.
Whereas neuromuscular blockade reversal with neostigmine and glycopyrrolate has unpredictable effects on blood pressure and heart rate, sugammadex has no adverse hemodynamic effects.
- 7.
Postsurgical hemorrhage may have a subtle presentation, requiring high clinical suspicion and frequent patient evaluation.
- 8.
Thromboelastography is a rapid point-of-care device that is used in the measurement of hemostasis.
- 9.
Direct oral anticoagulants are new medications with more predictable therapeutic effects compared to warfarin and have new reversal agents.
The postanesthesia care unit (PACU) traces its origin back to 1942 at the Mayo Clinic. This specialized unit is usually managed by the department of anesthesiology. During its daily operation, a designated anesthesiologist has the responsibility for making final medical decisions in the unit. PACU nurses have training in airway and basic life support management, as well as skill in the care of surgical wounds and drainage systems. The purpose of the PACU is to provide dedicated, centralized monitoring and nursing care to patients immediately after their operations before transferring them to a ward or intensive care unit (ICU) bed. A 1 : 1 patient-to-nurse ratio is required during the initial 15 minutes of a patient’s arrival to the PACU. During this crucial period, the patient has the highest risk for anesthesia-related complications. Discharge from the PACU to an ICU or ward is based on the modified Aldrete scoring system, a checklist in which a score of greater than 9 is required to transfer the patient ( Table 20.1 ).
| Discharge Criteria | Score |
|---|---|
| Activity: Ability to Move to Command or Spontaneously | |
| Four-extremity movement | 2 |
| Two-extremity movement | 1 |
| Zero-extremity movement | 0 |
| Respiration | |
| Able to deeply breathe or spontaneously cough | 2 |
| Dyspnea, shallow breathing, or limited breathing | 1 |
| Apnea | 0 |
| Circulation | |
| Blood pressure ± 20 mm Hg of baseline | 2 |
| Blood pressure ± 20–50 mm Hg of baseline | 1 |
| Blood pressure ± 50 mm Hg of baseline | 0 |
| Consciousness | |
| Fully awake | 2 |
| Arousal to sound or stimulation | 1 |
| Nonresponsive | 0 |
| Oxygen Saturation | |
| Maintains SpO 2 >92% on room air | 2 |
| Requires supplemental O 2 to keep SpO 2 >90% | 1 |
| O 2 saturation <90% despite supplemental O 2 | 0 |
a A score of ≥9 is required for postanesthesia care unit discharge.
Every patient admitted to the PACU requires an assessment for pain, airway patency, respiratory rate, oxygen saturation, heart rate and rhythm, and blood pressure. Depending on the severity of the patient’s condition, these vital signs are recorded every 5 minutes for the first 15 minutes and liberalized to every 15 minutes if the patient’s condition is favorable. The PACU is capable of providing more in-depth care if the patient’s condition warrants it. Arterial blood pressure monitoring with pulse-wave contour analysis can be performed to manage the causes of hemodynamic instability. Pulmonary artery pressure monitoring and transthoracic echocardiography can be performed at the bedside to assess volume status and cardiac function. Essentially, the PACU environment is capable of providing the highest level of care to meet the patient’s changing condition.
Postanesthesia care of patients with cardiac diseases is a complex and important topic that does not get the attention it deserves. Many patients with significant cardiac disease present for surgical procedures other than cardiac surgery. The type of operation and perioperative management influence the likelihood of postoperative cardiac complications in those with preexisting cardiac comorbidities. It is estimated that cardiac complications, such as myocardial infarctions (MIs) and cardiac arrests, can occur in up to 5% of patients undergoing noncardiac or nonvascular surgeries and up to 8% in vascular operations. The objective of this chapter is to address the common postoperative complications, their diagnoses, and management.
Surgery, Anesthesia, and the Heart
The intention of surgery is often to alleviate suffering, but its very process induces trauma. This controlled injury induces an inflammatory and stress response in the patient and leads to sympathetic nervous system activation, both of which may be detrimental to the patient with preexisting cardiac disease. The inflammatory process is driven by cytokines, including interleukin (IL)-1, IL-6, and tumor necrosis factor-α (TNF-α), which are released from activated macrophages after injury. During the acute phase of inflammation, there are increases in vascular dilation and permeability that are mediated by the release of histamine, serotonin, prostaglandin E 2 , leukotriene B4, and nitric oxide. This increased permeability allows for migration of plasma fluid that contains factors responsible for immunity, wound healing, and clotting. Depending on the severity of the inflammatory response, relative hypovolemia and hypotension can occur during and after surgery, with attendant risks to the patient.
During surgical stress, the neuroendocrine process is responsible for mediating volume and electrolyte balance. The posterior pituitary releases the hormone arginine vasopressin, which acts on the AVPR2 receptors in the kidneys, resulting in a rise in permeability at the distal collecting tubules and collecting ducts, allowing for increased water reabsorption and concentrated urine. Renin secretion results in aldosterone release, which enhances sodium and water reuptake in the distal collecting tubules. Together these neuroendocrine processes result in increased fluid retention and potentially increased circulating volume.
In addition to hormonal stimulation, the sympathetic autonomic nervous system is activated. The hypothalamus is responsible for stimulating catecholamine release from the adrenal medulla and presynaptic nerve terminals. The sympathetic effects of the released epinephrine and norepinephrine result in hypertension and tachycardia. The culmination of the inflammatory and sympathetic responses to stress leads to variations in hemodynamic and cardiac function (e.g., hypotension, hypertension, and tachycardia). In patients with cardiac disease, an unregulated response can precipitate myocardial ischemia or infarction, which often is first diagnosed in the PACU.
Inherent to surgery is the risk of blood loss, and to compensate for acute blood loss, the body has developed several adaptations. The systemic vascular resistance increases to maintain an appropriate mean arterial perfusion pressure, but this increase in afterload may come at the cost of decreased stroke volume and cardiac output in cardiac patients with poor left ventricular function. Blood flow is redistributed unequally, preferentially favoring high oxygen-extracting organs such as the heart and brain. During periods of anemia, the coronary arteries can increase their blood flow up to five times normal flow. Patients with heart disease, however, may not be capable of such compensation and may develop ischemia from oxygen deficit. Anemia caused by acute blood loss does not cause an immediate rightward shift of the oxygen dissociation curve (e.g., unloading of oxygen from hemoglobin). To decrease oxygen’s affinity for hemoglobin, it takes upwards of 12 hours for 2,3-DPG to be synthesized and produce a rightward shift of the curve. The decision to transfuse a patient should not be based solely on the value of the hemoglobin. A holistic view of the cardiac patient’s condition including ongoing blood loss, end-organ dysfunction, and increases in oxygen demand should guide the need to transfuse.
Postanesthesia Cardiac Complications in Cardiac Patients
Acute Coronary Syndrome
In patients with preexisting coronary artery disease (CAD), the narrowing of the coronary arteries is most commonly the result of atherosclerotic plaques. The size of the arterial occlusion will reduce the maximal flow of coronary blood to meet oxygen demand. When coronary oxygen demand outstrips oxygen delivery, angina pain can arise, and myocardial necrosis begins to occur. The postoperative period is a particularly dangerous time for patients with CAD because oxygen consumption can increase up to 50% from baseline, and the incidence of MI is as high as 5%.
Acute coronary syndrome is the term used to describe an acute reduction in coronary perfusion that results in cardiac impairment. The events that define this syndrome are unstable angina (UA)/non–ST segment elevation myocardial infarction (NSTEMI), and ST-segment elevation myocardial infarction (STEMI).
Unstable Angina/Non–ST Segment Elevation Myocardial Infarction
The development of UA/NSTEMI in the perioperative period is a result of multiple factors: a nonocclusive thrombus can form from plaque rupture, hypothermia can trigger coronary vasospasm that leads to impaired coronary blood flow, and myocardial ischemia can be precipitated from tachycardia as a result of pain, anemia, hypovolemia, and fever. The diagnosis of UA/NSTEMI is based on patient complaints, electrocardiography (ECG), and cardiac biomarkers. Patients presenting with UA/NSTEMI in the PACU may complain of substernal chest pain or pressure, with radiation to the jaw or arm or may have only subtle complaints, including midepigastric discomfort. What differentiates these symptoms from stable angina is that these symptoms occur spontaneously and are unprovoked, and there is an increase in frequency and severity. The 12-lead ECG is a critical diagnostic tool in this scenario. A finding of a prominent R wave with ST-segment depression of more than 0.5 mm or a T-wave inversion measuring greater than 1 mm in two contiguous leads is suggestive of UA/NSTEMI. The presence of cardiac biomarkers further differentiates angina pain caused by NSTEMI from UA. The creatine kinase-MB (CK-MB) has been a traditional biomarker for myocardial necrosis. It is, however, less sensitive than cardiac troponins because low levels of CK-MB have been detected in healthy humans and are also released when skeletal muscles are damaged. The troponin T and troponin I are specific to cardiac muscle. A rise in either troponin T or troponin I can be detected as early as 2 hours after the onset of symptoms or change in the ECG. Unlike CK-MB, the troponin levels can remain elevated for up to 14 days.
The medical treatment for UA/NSTEMI in the PACU is targeted toward the causes of increased oxygen demand. Supplemental oxygen should be administered to increase available systemic oxygenation. Shivering, which can increase total body oxygen consumption by up to 400%, should be treated with meperidine, if not contraindicated, along with surface-warming devices. Aggressive analgesic regimens should be used to treat acute postsurgical pain–induced hypertension and tachycardia. Acute blood loss and hypovolemia-induced ischemia should be treated with blood product administration and judicious fluid resuscitation. Stress-mediated tachycardia not caused by hypovolemia can be treated with β-blockade that allows for increased coronary perfusion time. Sublingual or intravenous (IV) nitroglycerin has been used for coronary vasodilation and to improve blood flow and relieve angina. Care should be taken in reducing systemic afterload and coronary perfusion pressure when administering nitrates. In addition, antiplatelet and anticoagulation therapy is aimed at preventing further coronary thrombus formation and can be used if surgical bleeding is not a concern. Aspirin is a first-line antiplatelet therapy in the treatment of UA/NSTEMI and can be started immediately. Clopidogrel is an alternative agent if patients are unable to tolerate aspirin therapy. Immediate dual-antiplatelet therapy with aspirin and clopidogrel or aspirin and ticagrelor is warranted if an invasive coronary intervention is planned. The American Heart Association/American College of Cardiology also recommends including anticoagulation therapy for the first 48 hours of symptom manifestation. Enoxaparin and unfractionated heparin are the first-line agents recommended, but fondaparinux is preferred for patients with increased risk of bleeding. Thrombolytics are contraindicated in the treatment of UA/NSTEMI because they have been associated with increased mortality rates. The administration of anticoagulation must be done with caution, being aware of the risks of anticoagulation in the setting of recent surgery, particularly in closed spaces (e.g., intraocular surgery). Multidisciplinary efforts including anesthesiology, cardiology, and surgery are essential for successful management (see Chapter 22 ).
Changes in the ECG tracing and positive cardiac biomarkers warrant cardiology consultation and close follow-up. Patients who are older than 65 years, present with prolonged chest pain, and have preexisting coronary stents, hemodynamic instability, or moderate renal insufficiency are considered to be at high risk for death. In these patients, there is benefit from early coronary angiography and intervention for obstructing lesions. In contrast, for lower risk patients, stress test evaluation in the form of an exercise stress test, radionucleotide myocardial perfusion scan, or pharmacologic stress test can be performed on a nonurgent basis. Coronary angiography in this group is done only if significant ischemia is seen during stress testing.
ST-Segment Elevation Myocardial Infarction
ST-segment elevation MI occurs when there is an abrupt cessation of coronary blood flow. The most common cause of an STEMI is lipid-rich atherosclerotic plaque rupture. This triggers the local release of serotonin, adenosine diphosphate, and epinephrine. These agents stimulate platelet aggregation and lead to coronary vessel obstruction. Coagulation factor activation forms fibrin-enhanced clots in the vessels that become resistant to thrombolysis. Thromboxane A 2 release further exacerbates MI through its powerful vasoconstricting properties. Less common causes of STEMI are severe coronary spasm, coronary arterial emboli, and coronary stent thrombosis.
The diagnosis of STEMI is based on the patient’s physical symptoms, ECG changes, rise in cardiac biomarkers, and echocardiography. The physical symptoms that patients in PACUs may exhibit are severe unrelenting substernal chest pain, anxiety, diaphoresis, and pallor. New rales may be auscultated in the lung fields, as well as new cardiac murmurs. The biomarkers CK-MB, troponin I, and troponin T all rise within 3 hours of the onset of the STEMI. A perioperative MI usually produces a rise in troponin to more than five times the top normal value of the laboratory. The degree of troponin I and troponin T rise is correlated with the degree of myocardial injury. ST-segment elevation on the ECG is considered significant if the height of the ST segment after the J-point is greater than 0.2 mV in men or 0.15 mV in women in the anterior leads or greater than 0.1 mV in all other leads. The location of the ST-segment elevation on a 12-lead ECG is useful in determining the culprit lesion(s) ( Table 20.2 ). Echocardiography also is helpful in the diagnosis of STEMI. Transthoracic echocardiography is capable of detecting regional wall motion abnormalities in acute MI, contractility dysfunction, and the presence of pericardial effusion.
| STEMI Type | Affected Coronary | ST-Segment Elevation Leads | Reciprocal Leads |
|---|---|---|---|
| Anterior | Left anterior descending | V 1 –V 6 | None |
| Posterior | Right circumflex | V 7 , V 8 , V 9 | R in V 1 –V 3 , ST depression in V 1 –V 3 |
| Inferior | Right coronary | II, III, aVF | I, aVL |
| Lateral | Left circumflex | I, aVL, V 5 , V 6 | II, III, aVF |
| Septal | Left anterior descending: septal arterial branches | V 1 –V 4 , absent Q wave in V 5 , V 6 | None |
| Right ventricle | Right coronary | V 1 , reversed V 4 | I, aVL |
a The most common type of ST segment elevation myocardial infarction (STEMI) is the inferior myocardial infarction (MI), with an incidence of 58%; the second most common is anterior MI, occurring 39% of the time.
The detection of STEMI requires immediate cardiology consultation for emergent coronary angiography and reestablishment of coronary blood flow. The immediate medical treatment is similar to the treatment of UA/NSTEMI. IV opioids should be used to treat angina pectoris and to reduce the sympathetic stress response that can increase myocardial oxygen demand. Dual-antiplatelet therapy with either aspirin and clopidogrel or aspirin and prasugrel is used to reduce thrombus formation, if not surgically contraindicated. In STEMI patients without evidence of cardiogenic shock, administration of β-blockers can reduce infarct size, suppress arrhythmias, and relieve chest pain from increased myocardial oxygen demand. Thrombolytic therapy with tenecteplase or tissue plasminogen activator is reserved for centers that lack immediate access to a coronary catheterization laboratory. It is recommended that therapy be initiated within 12 hours of the onset of symptoms. In immediate postsurgical patients, the risks of thrombolytic therapy should be strongly considered. Surgical site bleeding, gastrointestinal bleeding, and most devastating of all, intracranial hemorrhage can arise from this therapy.
Coronary angiography and percutaneous coronary intervention (PCI) should occur within 90 minutes of the diagnosis of STEMI. PCI with drug-eluting stents is indicated for patients presenting with two or fewer culprit lesions. Presently, some interventional cardiologists perform PCI on patients with left main CAD because the safety profile has been shown to be comparable to coronary artery bypass grafting (CABG). Patients in cardiogenic shock can be supported temporarily with percutaneous mechanical support. The intraaortic balloon pump (IABP) has been in use since the 1960s and is able to reduce myocardial oxygen demand by increasing coronary perfusion pressure, reducing arterial systemic afterload, and providing up to 0.5 L/min of cardiac output. The Abiomed Impella is a percutaneous ventricular assist device that is inserted retrograde through the femoral artery, traverses the aortic valve, and sits in the left ventricle (LV). A small axial pump pulls blood from the LV and expels up to 4 L/min of flow into the ascending aorta. For patients with biventricular failure after a STEMI, venoarterial extracorporeal membrane oxygenation (VA-ECMO) can be used to deliver 5 L/min of oxygenated blood. All of these devices can be inserted in the catheterization laboratory during coronary angiography and intervention.
In patients found to have three or more coronary arteries diseased, CABG has been found to be superior to PCI for long-term survival. Referral for emergent CABG can occur when coronary angioplasty has failed, coronary dissection occurs during percutaneous intervention, or MI-induced ventricular septal rupture or mitral regurgitation and posterior wall MI are present. Although CABG has been shown to have superior long-term survival rates compared with PCI, emergent surgical revascularization has significantly higher mortality rates in the first week after surgery.
Acute Decompensated Heart Failure
Decompensated heart failure (HF) is defined as the heart’s inability to deliver oxygenated blood to meet the body’s metabolic needs. For patients in the PACU presenting with acute decompensated HF, the causes include volume overload, pressure overload, and acute contractility dysfunction. Increases in preload from fluid administration may precipitate HF symptoms (shortness of breath, hypoxemia, pulmonary congestion, peripheral edema, alteration in mental status, and end-organ dysfunction) from the inability of the LV to increase stroke volume caused by reduced myocardial contractility. Sympathetic stress responses from surgical pain lead to arterial vasoconstriction and result in an increase in afterload. The LV in patients with reduced myocardial contractility is unable to overcome the high resistance, leading to a reduction in stroke volume and symptoms of acute HF. The causes of new-onset contractility failure can be the result of MI and cardiac valve impairment.
The diagnosis of acute HF can be made by presenting symptoms, biochemical findings, and imaging studies. A PACU patient with acute-onset HF may complain of dyspnea or orthopnea and require an increase in supplemental oxygen. Physical findings are notable for rales on pulmonary auscultation, presence of jugular venous distention, and cold and clammy extremities from decreased perfusion. The biomarkers B-type natriuretic peptide (BNP) and N-terminal fragment pro-BNP (NT-proBNP) are used in the diagnosis of HF because values of 500 pg/mL or greater and 300 pg/mL or greater, respectively, have a 90% positive predictive value. Obtaining a complete metabolic panel is helpful in assessing liver and renal dysfunction from venous congestion and poor perfusion. In addition, the laboratory findings are helpful in the identification of electrolyte abnormalities such as hyponatremia and hypokalemia. Transthoracic echocardiography is a powerful imaging tool that provides real-time information both visually and numerically of the heart’s chamber size, thickness, and systolic and diastolic function, as well as the presence of any structural abnormality. This information can provide a diagnosis as well as guide therapy. Chest radiography may demonstrate pulmonary venous congestion, interstitial edema, and cardiomegaly. It should be noted, however, that these findings may not manifest while the patient is in the PACU. Radiographic findings generally are delayed by up to 12 hours from the onset of clinical symptoms.
The treatment of acute HF in the PACU is directed to its cause. Agents such as loop diuretics reduce preload and diastolic ventricular wall stress and can optimize myocardial contractility. For patients with signs of volume overload, diuretics provide symptomatic relief by quickly reducing pulmonary and peripheral congestion. For patients with pressure overload–induced HF symptoms, afterload-reducing agents such as nicardipine, clevidipine, nitroprusside, and hydralazine will lower the resistance against which the heart must contract. As a result of vascular smooth muscle relaxation, stroke volume and cardiac output will increase. The inodilators dobutamine and milrinone should be considered in patients with worsening HF symptoms who have been refractory to the treatments described. These agents are able to increase contractility and reduce systemic vascular resistance, leading to improved cardiac output and systemic perfusion. In acute HF, care should be taken to avoid any agents that can reduce contractility, such as β-blockers. When there is an escalation in symptoms or treatment, a cardiologist should be consulted, as well as consideration for transferring to a facility with a higher level of care (i.e., ICU), if needed.
Medical therapy can be considered a failure should patients continue with altered mental status; cold, clammy extremities; rising lactate level; and worsening end-organ dysfunction. In this situation, temporary percutaneous mechanical circulatory support is necessary with such devices as the IABP, Abiomed Impella, and VA-ECMO. Each device is capable of providing left ventricular support during cardiogenic shock from acute HF. VA-ECMO is unique in that it can provide biventricular support. In patients with acute renal failure and fluid overload, consultation with a nephrologist for renal replacement therapy and volume removal also is prudent.
Arrhythmias
The heart’s conduction system is composed of a network of excitable cells that transmit electrical impulses, resulting in organized and rhythmic contractions. Abnormalities in impulse generation and conduction are responsible for the development of arrhythmias. The ECG remains the most essential tool in the diagnosis and management of these electrical abnormalities (see Chapter 9 ).
Tachyarrhythmias are cardiac rhythms that have a rate greater than 100 beats/min. Sinus tachycardia is the most common arrhythmia, with a heart rate ranging from 100 to 160 beats/min. This arrhythmia is a sympathetic-mediated hastening of the sinoatrial node. Pain, hypovolemia, and stimulants can trigger this rhythm. On ECG, the QRS complex is normal, and the sole abnormality is a fast rate. Treatment is directed toward the triggering cause of the sinus tachycardia.
Supraventricular tachycardia (SVT) is a paroxysmal, regular, and narrow-complex tachycardia (QRS <140 ms) with a rate between 140 and 280 beats/min. The most common form of SVT is atrioventricular nodal reentrant tachycardia (AVNRT). In AVNRT, the functional reentry circuit occurs within the atrioventricular (AV) node. Patients in the PACU presenting with this arrhythmia often complain of rapid palpitations, dyspnea, and presyncopal events. The treatment for SVT depends on the patient’s condition. In a hemodynamically stable PACU patient (defined as a mentally alert patient with a perfusing heartbeat, and a mean arterial pressure sufficient to perfuse end organs), vagal maneuvers in the form of a Valsalva or carotid massage can be attempted. If these maneuvers fail or the patient is unstable, adenosine, a transient AV nodal blocking agent, should be administered intravenously. Secondary options for chemical treatment include an IV calcium channel blocker, diltiazem, or β-blocker such as metoprolol or esmolol.
Atrial fibrillation is an irregularly irregular narrow-complex tachycardia with rates between 110 to 180 beats/min. On ECG, there is an absence of a P wave, and the QRS complex is narrow and has an irregular rhythmic pattern. The aberrant conduction abnormality occurs in the atria and in portions of the pulmonary vein caused by reentrant circuits and electrical spiral waves in which the tissue lacks a refractory period. Risk factors for the development of atrial fibrillation include cardiac ischemia, hyperthyroidism, mitral valve disease, excessive alcohol use, pericarditis, and pulmonary embolism. In patients presenting with new-onset atrial fibrillation who are hemodynamically stable, the goal is to achieve ventricular rate control, targeting a rate of less than 110 beats/min. Agents such as metoprolol and diltiazem are effective pharmacologic therapy to achieve this goal. Pharmacologic cardioversion using an IV amiodarone bolus followed by a continuous infusion for 24 hours has a conversion to sinus rhythm success rate ranging from 55% to 95%. Patients presenting with new-onset atrial fibrillation and hemodynamic instability should immediately receive direct-current synchronized cardioversion set to 100 to 200 J. A transesophageal echocardiogram should be obtained to confirm the absence of an atrial thrombus before electrical cardioversion. Sedation or anesthesia should be considered in the PACU.
Atrial flutter presents with a sawtooth pattern on ECG caused by the presence of rapid P-waves. The QRS complex can appear regular or irregular depending on the presence of an AV conduction block. During atrial flutter, the atrial rate can be as high as 350 beats/min. The ventricular rate can be as high as 150 beats/min. A reentrant circuit in the atria is responsible for the triggering of the arrhythmia and is strongly associated with the presence of structural heart disease. The therapeutic agents used in atrial fibrillation are helpful in reducing the ventricular rate in atrial flutter but have a poor success rate in converting the patient to sinus rhythm. Electrical cardioversion is reserved for the hemodynamically unstable patient.
Premature ventricular contractions (PVC) originate from foci below the AV node. Stress, pain, stimulants, hypomagnesemia, and hypokalemia can trigger a PVC. In isolation, a PVC is benign. With multiple PVCs, the PACU patient may complain of palpitations and near syncope. A PVC occurring on the T wave, corresponding with ventricular repolarization, can trigger ventricular fibrillation or torsades de pointes, requiring immediate corrective action (i.e., defibrillation and magnesium sulfate administration). The initial treatments of PVCs consist of replacing electrolytes and discontinuation of proarrhythmic drugs. If the symptoms persist, lidocaine, β-blockers, and amiodarone are effective therapeutic agents.
Ventricular tachycardia (VT) is defined as three or more consecutive PVCs occurring at a heart rate of greater than 120 beats/min. On ECG, repetitive wide QRS complex and absent P waves are the typically observed features. VT may occur spontaneously in patients with systolic ejection fractions of 35% or less as a result of QT–prolonging medications or electrolyte depletion or in ischemic and structural heart disease. In patients with VT who are hemodynamically stable, medical therapy with amiodarone is appropriate. Further therapies should be targeted toward removing triggers. Patients who present in unstable monomorphic VT require immediate cardioversion. Synchronized cardioversion decreases the risk of the monomorphic VT degenerating to ventricular fibrillation. In polymorphic VT and pulseless VT, Advance Cardiac Life Support (ACLS) should begin immediately, with defibrillation at 360 J with a monophasic defibrillator.
Ventricular fibrillation (VF) is a lethal rhythm if timely intervention is not performed. VF correlates to unorganized ventricular contraction and the loss of stroke volume and cardiac output. Initial management of VF is to initiate the most current ACLS protocol. Chest compressions should be started immediately for systemic perfusion. Defibrillation should be applied as soon as possible. If electrical therapy fails, alternating doses of IV epinephrine and vasopressin should be administered. During resuscitative efforts, the anesthesiologist should identify and treat the inciting event (e.g., hyperkalemia, iatrogenic drug administration, acidosis, or hypoxemia).
Bradyrhythmias include abnormal conduction with rates less than 60 beats/min. Sinus bradycardia occurs any time a regular heart rhythm is below 60 beats/min. Excessive vagal tone, nodal blocking agents, and neuraxial blockade from a paravertebral block or thoracic epidural can contribute to its manifestation. In asymptomatic patients, no treatment is required. Patients presenting with β-blocker or calcium channel blocker overdose can be reversed with glucagon or β-agonists. Neuraxial blockade–induced bradycardia can be treated with ephedrine. If hypotension, bradycardia, and altered mental status occur, epinephrine or dopamine infusions can alleviate symptoms. A cardiology consultation should be obtained for any PACU patient with persistent and symptomatic bradycardia because cutaneous or transvenous pacing may be required.
Disruption of AV conduction occurs with third-degree heart block. There is complete dissociation of electrical impulses from the atria to the ventricles. As a result, the QRS complex is wide, and the rate is 30 to 45 beats/min. Patients with third-degree heart block may present with weakness, dyspnea, or syncope. Aside from a cardiology consultation, immediate treatment includes transcutaneous or transvenous pacing, depending on the facility’s capability, or pharmacologic stimulation with isoproterenol infusion.
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