Hypotension is a common postoperative complication that can result from hypovolemia, decreased systemic vascular tone, and/or reduced cardiac output. Hypotension can result in myocardial ischemia or infarction, stroke, acute renal failure, and bowel ischemia. During hypotension, the body attempts to redirect blood flow toward the brain, heart, and kidneys: Signs of hypoperfusion of these organs suggest that compensatory mechanisms have failed. Hypotension may be defined as a more than 20% decline of blood pressure from baseline or evidence of end-organ hypoperfusion.
Accurate measurement of blood pressure is essential to making a correct diagnosis of hypotension. An inappropriately large blood pressure cuff or an arterial transducer that is improperly zeroed, positioned, or dampened will provide falsely low blood pressure readings.
Causes of hypovolemia in the PACU include inadequate fluid replacement, ongoing hemorrhage, and fluid sequestration ("third spacing"). Clinical evaluation of a patient's intravascular volume status requires consideration of preoperative status and comorbid conditions, type and duration of surgery, estimated blood loss, fluid replacement, and evidence of hemostasis. Signs of hypovolemia include hypotension, tachycardia, orthostasis, decreased skin turgor, oliguria, and dry mucous membranes. Administration of a fluid bolus during the initial assessment is generally a safe maneuver. Persistent hypotension despite seemingly adequate fluid replacement requires further assessment and may require monitoring of central venous and pulmonary artery pressures or echocardiography.
Neuraxial anesthesia, residual inhalation agents, administration of vasodilators, rewarming after hypothermia, transfusion reactions, systemic inflammation, and sepsis can cause hypotension by decreasing systemic vascular resistance and impairing venous return. Hypovolemia increases systemic hypotension due to vasodilatation, but fluid resuscitation often does not fully restore the blood pressure. Pharmacologic treatment includes administration of a peripheral vasoconstrictor. A pure α1-agonist, such as phenylephrine, often is chosen because it is unlikely to cause dysrhythmias and can be administered through a peripheral intravenous line. More potent pressor agonists, such as norepinephrine, usually require central venous access for administration. Diagnosis and treatment of the specific etiology of the vasodilatation should be concurrent with symptomatic treatment.
Myocardial Ischemia and Infarction
A variety of factors in the perioperative period may alter the balance between myocardial O2 supply and demand. The body's physiologic response to surgery is an increase circulating catecholamines; these increase myocardial demand by increasing heart rate, myocardial contractility, and peripheral vascular resistance. Myocardial O2 supply may be decreased by perioperative factors such as hypoxemia and hypotension. Patients with coronary artery disease or those at risk for coronary disease have significantly higher rates of perioperative myocardial ischemia, infarction, and cardiac death.34 Mangano et al35 reported that the incidence and severity of perioperative myocardial ischemia was greatest during the first 48 hours after surgery. Badner et al36 reported the peak incidence of perioperative myocardial infarction (MI) occurred during the first 24 hours following surgery.
The diagnosis of perioperative ischemia can be difficult because often the condition is silent. Postoperative chest pain may be masked by residual anesthesia or analgesics, and pain perception may be altered by the competing stimulus of incisional pain. The patient at high risk for perioperative myocardial ischemia and infarction should be assessed by ECG preoperatively, immediately after surgery, and on the first 2 postoperative days.37 In patients with ECG changes or chest pain typical of an acute coronary syndrome, serial markers of myocardial injury (troponin, creatine phosphokinase) should be followed. Therapy for perioperative ischemia or MI is similar to that for other medical patients with MI and includes aggressive pain control, β-blockade, aspirin, and nitrates. Administration of anticoagulants is generally reserved for cases of acute coronary stent thrombosis or ST elevation MI and requires weighing the risks of surgical bleeding with the benefits of anticoagulation.
Cardiac dysrhythmias are common during the perioperative period; transient dysrhythmias reportedly occur in 62% to 84% of patients.38 Most perioperative dysrhythmias are benign. They are most likely to occur in patients with underlying structural heart disease; however, the precipitating factor is usually a transient event such as hypoxia, ischemia, increased circulating catecholamine levels, altered acid–base status, or electrolyte abnormalities. The clinical significance of a dysrhythmia depends on the patient's underlying cardiac function. Bradycardia may cause a clinically significant reduction in cardiac output in a patient with relatively fixed stroke volume. Tachycardia may reduce cardiac output by decreasing diastolic filling time and increasing myocardial O2 consumption, resulting in myocardial ischemia. Loss of atrial contraction in atrial fibrillation may decrease cardiac output by decreasing diastolic filling. The management strategy for a new dysrhythmia is focused on stabilizing hemodynamics and treating the underlying problem. Significant hemodynamic instability that results from dysrhythmia is an indication for emergent cardioversion.
Specific antiarrhythmic therapy in the postoperative setting is similar to that in the nonoperative setting, but generally therapy will not be effective unless the precipitating factors are identified and treated.
Tachyarrhythmias usually are classified according to their anatomic origin as either supraventricular or ventricular. Supraventricular arrhythmias include sinus tachycardia, atrial fibrillation and flutter, ectopic atrial tachycardia, multifocal atrial tachycardia, junctional tachycardia, atrioventricular nodal reentrant tachycardia, and accessory pathway reciprocating tachycardias. Ventricular arrhythmias consist of ventricular premature beats, ventricular tachycardia, and ventricular fibrillation. For a comprehensive discussion of cardiac arrhythmias, see Chapters 44 and 51.
Sinus tachycardia is the most common dysrhythmia in the immediate postoperative period. Increased sympathetic discharge resulting from pain, hypovolemia, anemia, anxiety, hypoxia, and hypercarbia are common causes. Sinus tachycardia usually is benign; however, it may precipitate myocardial ischemia in a patient with coronary artery disease. Treatment of the underlying cause(s) (eg, analgesics for pain, intravenous fluids for hypovolemia, sedatives for anxiety) usually is adequate for resolution. In patients at risk for myocardial ischemia, β-blockade usually is effective in reducing the heart rate.
Supraventricular tachyarrhythmias are more common after thoracic surgery than after other types of noncardiac surgery with a reported incidence of 15% or more.39 In these patients, prophylaxis with calcium channel blockers or β-blockers significantly reduces the occurrence of atrial fibrillation.39
Atrial fibrillation is the most common supraventricular dysrhythmia after both cardiac and noncardiac surgery and has the greatest potential for serious consequences.40,41 For unstable patients with atrial fibrillation and a rapid ventricular rate, urgent cardioversion is indicated. In hemodynamically stable patients, β-blockers, calcium channel blockers, or amiodarone are alternatives for rate control. In most patients, atrial fibrillation resolves within 36 to 48 hours. New-onset atrial fibrillation raises increased risk of stroke from cerebral embolism; anticoagulation may not be possible in a postoperative patient at risk for bleeding.
Bradycardia usually is associated with sinus node or atrioventricular node dysfunction. The various possible presentations are sinus bradycardia, sinus pause, sinoatrial block, sinus arrest, junctional rhythms, and varying degrees of heart block. At sufficiently slow heart rates, ventricular escape beats may be seen. In the postoperative setting, bradycardia is often due to increased vagal tone as a result of hypoxemia, pain, nausea, drugs (eg, neostigmine, β-blockers, or opioids) or the effects of neuraxial anesthesia. Sinus bradycardia can be a normal rhythm in a young healthy patient. Bradycardia without hypotension usually is benign and no treatment is necessary. If bradycardia is associated with hemodynamic compromise (hypotension, low cardiac output), treatment with antimuscarinic agents (glycopyrrolate or atropine) or β-agonists (ephedrine) can restore normal sinus rhythm.
Development of complete heart block can occur in patients with preexisting conduction disorders, and the resulting idioventricular bradycardia often compromises systemic hemodynamics. Treatment includes atropine to improve atrioventricular nodal conduction and permit supraventricular impulse transmission, or epinephrine, isoproterenol, or ventricular pacing to increase ventricular rate. In the setting of complete heart block, the need to provide either external or internal pacing must be anticipated; consultation with a cardiologist in anticipation of requirement for pacing is recommended.
Ectopic beats, whether atrial or ventricular, are common and by themselves do not necessarily imply underlying cardiac disease. In the postoperative period, ectopic beats often are associated with electrolyte imbalances, hypoxia, acid–base abnormalities, and hypertension. They may result from drug therapy (eg, digitalis toxicity) or cardiac irritation from central venous catheters. Hypokalemia and hypomagnesemia are the most common electrolyte abnormalities associated with ectopy. Care should be taken when correcting these abnormalities because rapid administration of large quantities of either potassium or magnesium can produce hemodynamic and rhythm disturbances more deleterious than simple ectopy.
Frequent premature atrial contractions are usually of minor hemodynamic significance but may be harbingers of supraventricular tachycardia or atrial fibrillation. Medical therapy is generally not needed, but patients should be monitored closely.
Similarly, premature ventricular contractions in an asymptomatic patient generally do not require treatment. Preoperative ventricular ectopy usually reoccurs postoperatively and does not predict an adverse outcome.42
Postoperative ECG Changes
ECG changes are common after anesthesia and surgery. Changes in P- or T-wave morphology, intraventricular conduction, or ST segments may occur in the absence of a cardiac abnormality or ischemia. These changes can result from cardiac effects of anesthetics and other drugs, increased sympathetic tone, hypothermia, and electrolyte imbalances. Breslow et al43 reported an 18% incidence of T-wave changes in a postoperative population; changes occurred with equal frequency in all age groups and were not more common in patients with preexisting coronary artery disease. These patients did not demonstrate any evidence of postoperative myocardial ischemia or injury, and most of the ECG changes resolved with 24 hours. If there is a suspicion of perioperative ischemia, T-wave changes should be treated as a potential MI; therapeutic control of heart rate and blood pressure, serial ECGs and cardiac enzyme levels, as well as a cardiology consultation are indicated.
Hypertension is a very common problem in the postoperative period. Typical onset is early, usually within 2 hours after surgery, and generally requires treatment for 6 hours or less. It occurs most commonly after vascular, head and neck, and neurosurgical procedures (Table 71-3).44 Patients with preexisting hypertensive disease are more likely to develop postoperative hypertension, especially if antihypertensive medications are withheld preoperatively. Noxious stimuli, including pain, anxiety, bladder distension, fluid overload, hypoxemia, hypercarbia, and hypothermia, activate the sympathetic nervous system producing hypertension. Complications of severe postoperative hypertension include myocardial ischemia/infarction, dysrhythmias, congestive heart failure, stroke, and increased surgical bleeding.
Table 71-3 Frequency of Acute Postoperative Hypertension by Surgical Procedure ||Download (.pdf)
Table 71-3 Frequency of Acute Postoperative Hypertension by Surgical Procedure
|Abdominal aortic surgery||33-75|
|Radical neck dissection||10-20|
|Elective general surgery||3-20|
|Flexion contracture release||46|
The decision to treat hypertension requires consideration of the patient's baseline blood pressure, coexisting diseases, and perceived risk of complications: systolic or diastolic blood pressure more than 20% above baseline, signs or symptoms of complications such as chest pain or dysrhythmias, or a perceived increased risk of complications are indications for treatment.45 Reversible causes of hypertension (eg, pain, anxiety, bladder distension) should be ruled out before initiation of antihypertensive therapy. For patients with preexisting hypertension, resumption of chronic antihypertensive therapy is a sensible option. Short-term control of blood pressure in the PACU is best accomplished with drugs that have a rapid onset and possess a short to intermediate duration of action. Intravenous agents such as labetalol, esmolol, propranolol, and hydralazine are commonly used for short-term control of blood pressure. For persistent or refractory hypertension, continuous infusions of vasodilators such as nitroprusside, nitroglycerin, nicardipine, or fenoldopam may be required.