Hypotension is a significant decrease of arterial blood pressure below the patient’s usual range. It may be due to a decrease in cardiac function (contractility), systemic vascular resistance (SVR or afterload), venous return (preload), or to the presence of dysrhythmias.

1. Most anesthetic agents, including inhalational agents, barbiturates and benzodiazepines (see Chapter 12) cause dose-dependent direct myocardial depression. Opiates are not direct myocardial depressants in usual clinical doses, though clinically significant bradycardia and hypotension may be observed due to decreased sympathetic outflow.

2. Cardiac medications such as β-adrenergic antagonists, calcium channel blockers and lidocaine, are myocardial depressants.

3. Acute cardiac dysfunction may occur with myocardial ischemia or myocardial infarction (MI), hypocalcemia, severe acidosis or alkalosis, hypothermia of less than 32°C, cor pulmonale, vagal reflexes, and systemic toxicity from local anesthetics (particularly bupivacaine).

1. A decrease in SVR can be seen with many of the drugs administered during anesthesia.

a. Isoflurane and, to a lesser extent, sevoflurane and desflurane produce a dose-dependent decrease in SVR.

b. Opiates and propofol produce loss of vascular tone by reducing sympathetic nervous system outflow.

c. Benzodiazepines may decrease SVR, particularly when administered at high doses in conjunction with opiates.

d. Direct vasodilators (e.g., nitroprusside, nitroglycerin, and hydralazine).

e. α₁-Adrenergic blockers (e.g., droperidol, chlorpromazine, phentolamine, and labetalol).

f. α₂–Adrenergic agonists (e.g., clonidine).

g. Histamine-releasing medications (e.g., d-tubocurarine, mivacurium, and morphine).

h. Ganglionic inhibitors (e.g., trimethaphan).

i. Calcium channel blockers.

j. Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers.

k. Inodilators (e.g., milrinone).

2. Sympathetic blockade frequently occurs during spinal and epidural anesthesia, leading to a reduction in SVR.

3. Sepsis causes release of vasoactive substances that mediate peripheral vasodilation and cause hypotension.

4. Vasoactive metabolites released during bowel manipulation, aortic cross-clamp release, or tourniquet release may cause hypotension.

5. Allergic reactions (see section XVIII) may cause profound hypotension.

7. Adrenal insufficiency (including iatrogenic causes)

1. Hypovolemia may be caused by blood loss, insensible evaporative losses, preoperative deficits (e.g., nothing-by-mouth status, vomiting, diarrhea, nasogastric tube suction, enteric drains, and certain bowel preparations), or polyuria (e.g., diuretic use, diabetes mellitus, diabetes insipidus, or postobstructive diuresis). In patients undergoing positivepressure ventilation changes in the intra-arterial blood pressure trace are correlated with volume responsiveness. Hypovolemia can be considered when the delta-down component (the difference between the systolic blood pressure during apnea and the lowest systolic blood pressure after a positive pressure breath) of the systolic pressure variation is greater than about 10 mm Hg in a paralyzed and mechanically ventilated patient.

2. Caval compression may result from a gravid uterus, massive ascites, tumor, surgical maneuvers or during laparoscopic insufflation of greater than 10 mm Hg leading to increased intra-abdominal pressure.

3. Increased venous capacitance may occur with the following:

a. Sympathetic blockade (e.g., ganglionic blockers or regional anesthesia)

b. Direct vasodilators (e.g., nitroglycerin)

c. Histamine-releasing medications (e.g., morphine, mivacurium)

d. Medications that reduce sympathetic outflow (e.g., propofol, inhalational agents, and opioids).

4. Increased intrathoracic pressure will impair venous return. Possible causes include tension pneumothorax (section XIII), mechanical ventilation with large tidal volumes, positive end-expiratory pressure (PEEP), auto-PEEP (air trapping or dynamic hyperinflation) and continuous positive airway pressure (CPAP).

5. Acute primary increases in central venous pressure (CVP) can cause a decrease in venous return as the increased CVP reduces the pressure gradient that drives blood from the periphery into the right heart.

a. Tension pneumothorax leads to compression of the heart and great vessels. The resulting elevation in CVP decreases preload and gives rise to hypotension.

b. Cardiac tamponade is a collection of fluid in the pericardial space causing compression of the heart, resulting in decreased filling due to elevated intrapericardial pressures.

c. Pulmonary embolism obstructs right ventricular ejection and in turn raises right atrial pressure, which can drastically reduce venous return.

d. Intra-abdominal hypertension causes increased intrathoracic pressure which then compresses the heart and raise the CVP. Thus the CVP can be elevated while the heart is severely underfilled.

1. Tachydysrhythmias often result in hypotension secondary to a decreased diastolic filling time.

2. Atrial fibrillation, atrial flutter, and junctional rhythms cause hypotension from loss of the atrial contribution to diastolic filling. This is particularly pronounced in patients with valvular heart disease or diastolic dysfunction, in whom atrial contraction may augment end-diastolic volume by more than 30%.

3. Bradydysrhythmias may cause hypotension if preload reserve is inadequate to maintain a compensatory increase in stroke volume.

E. Treatment of hypotension should be directed toward correcting the underlying cause. Depending on the etiology, appropriate maneuvers include:

2. Volume expansion (e.g., administration of blood products, colloids or crystalloids)

3. Vasopressor support to increase vascular resistance or decrease venous capacitance (e.g., phenylephrine and vasopressin if acidemic) and increase stroke volume (e.g., epinephrine).

4. Correction of mechanical causes, such as relief of pericardial tamponade, placement of a needle thoracostomy and chest tube for pneumothorax, reducing or eliminating PEEP or CPAP, decreasing mean airway pressure, relieving obstruction of the vena cava (e.g., left uterine displacement for a pregnant patient), surgically relieving intraabdominal hypertension, or surgically removing a massive pulmonary embolism.

5. Antidysrhythmic (see section III) may include β-blockers, calcium channel blockers, and amiodarone.

6. Inotropic support (e.g., dobutamine, dopamine, norepinephrine, milrinone, and epinephrine).

7. Anti-ischemic therapy may include raising the systemic blood pressure with vasopressors and then treating the underlying ischemic myocardium (see section XIV).

8. In the case of refractory hypotension, consider the use of additional noninvasive monitors (e.g., transthoracic or transesophageal echocardiography) and the placement of invasive monitors (e.g., arterial line, central venous catheter or pulmonary artery catheter) to aid diagnosis.

1. Catecholamine excess may be seen with inadequate anesthesia, especially during laryngoscopy, intubation, incision, emergence, hypoxia, hypercarbia, patient anxiety, pain, and prolonged tourniquet use.

2. Preexisting disease such as essential hypertension or pheochromocytoma.

4. Systemic absorption of vasoconstrictors such as epinephrine and phenylephrine.

5. Aortic cross-clamping which leads to a significant increase in SVR.

6. Rebound hypertension from discontinuation of clonidine or β-adrenergic blockers.

7. Drug interactions. The administration of ephedrine to patients receiving tricyclic antidepressants (e.g., amitriptyline, nortriptyline, doxepin) and monoamine oxidase inhibitors (e.g., isoniazid, rasagiline, selegiline) may cause an exaggerated hypertensive response.

9. Administration of indigo carmine dye (via an α-adrenergic effect).

B. The treatment of hypertension is directed toward correcting the underlying cause. It may include the following:

1. Improving oxygenation and ventilation.

2. Increasing the depth of anesthesia (e.g., volatile and IV anesthetics and analgesics).

3. Sedating an anxious patient or emptying a full bladder.

4. Medications (for further discussion, see Chapter 20).

a. Combined α and β-Adrenergic blocking agents: labetalol in 5 to 10 mg increments intravenously [IV].

b. β-Adrenergic blocking agents: propranolol, 0.5- to 1.0-mg increments IV; metoprolol, 1.0-5.0 mg IV; or esmolol, 5- to 10-mg increments IV.

c. Vasodilators: hydralazine, 2.5- to 5-mg increments IV; nitroglycerin infusion, starting at 30 to 50 µg/minute IV and titrating to effect; nitroprusside infusion, 30 to 50 µg/minute IV and titrating to effect.

d. Calcium channel blockers: verapamil, 2.5 to 5 mg IV; diltiazem, 5 to 10 mg IV.

A. Sinus bradycardia is a sinus node-driven heart rate of less than 60 beats/minute. Unless there is severe underlying heart disease, hemodynamic changes are minimal. With very slow rates, atrial and ventricular ectopic escape beats or rhythms may occur.

b. Intrinsic cardiac disease such as sick sinus syndrome or acute MI (particularly inferior wall MI).

c. Medications such as succinylcholine (especially in young children via a direct cholinergic effect), anticholinesterases, β-adrenergic blockers, calcium channel blockers, digoxin, and synthetic narcotics (e.g., fentanyl and remifentanil).

d. Increased vagal tone occurs with traction on the peritoneum or spermatic cord; pressure on the globe via the oculocardiac reflex; pressure near the brainstem during craniotomies for posterior fossa lesions; direct pressure on the vagus nerve or carotid sinus during neck or intrathoracic surgery; acute distension of the peritoneal cavity during laparoscopy; centrally mediated vagal response from anxiety or pain (vasovagal reaction); and valsalva maneuvers.

a. Verify adequate oxygenation and ventilation.

b. Bradycardia due to increased vagal tone requires discontinuation of the provocative stimulus. Atropine (0.5 mg IV) or low-dose epinephrine (10 to 50 µg IV) may be needed if the patient is hypotensive. Glycopyrrolate (0.2 to 0.6 mg IV) or ephedrine (5 to 10 mg IV) may be given for hemodynamically stable bradycardia, the latter may be more appropriate for settings of brief surgical stimulation of the vagus.

c. In patients with intrinsic cardiac disease, treatment should proceed with atropine (0.5 mg IV), chronotropes (e.g., ephedrine, dopamine), or cardiac pacing.

B. Sinus tachycardia is a sinus node-driven heart rate greater than 100 beats/minute. The rate is regular and rarely exceeds 160 beats/minute. Electrocardiogram (ECG) should demonstrate a P wave preceding each QRS complex with a fixed PR interval.

1. Etiologies include catecholamine excess, inadequate anesthesia or analgesia; hypercarbia; hypoxia; hypotension; hypovolemia; medications (e.g., pancuronium, desflurane, atropine, and ephedrine); fever; MI; pulmonary embolism; tamponade; tension pneumothorax; malignant hyperthermia; pheochromocytoma; and thyrotoxicosis.

2. Treatment should be directed toward correcting the underlying cause and may include the following:

a. Correcting oxygenation and ventilation abnormalities.

b. Increasing the depth of anesthesia and treating pain with analgesics.

c. Correcting hypovolemia.

d. Medications such as opioids and β-adrenergic blockers. Patients with active coronary artery disease and adequate blood pressure may benefit by treatment with β-adrenergic blockers to control the heart rate while the cause is being determined.

1. First-degree atrioventricular (AV) block is characterized by a PR interval of 0.2 seconds or longer. In first-degree block, every atrial pulse is transmitted to the ventricle.

2. Second-degree AV block is divided into two types: Mobitz type 1 (Wenckebach) and Mobitz type 2.

a. Mobitz type 1 (Wenckebach) usually occurs when a conduction defect is in the AV node and is manifest by a progressive PR prolongation culminating in a nonconducted P wave. It is generally benign.

b. Mobitz type 2 is a conduction defect in or distal to the AV node. It presents with a constant PR interval and frequent nonconducted P waves. It is more likely to progress to third-degree block.

3. Third-degree AV block (complete heart block) is usually due to lesions distal to the His bundle and is characterized by the absence of AV conduction. Usually, a slow ventricular rate is seen (fewer than 45 beats/minute). P waves occur regularly but are independent of QRS complexes (AV dissociation).

4. Treatment of heart block

a. First-degree AV block does not usually require specific treatment, however, temporary pacing should be available in the case of first-degree heart block in combination with a bifascicular block (so-called “trifascicular block”).

1. Mobitz type 1 requires treatment only if symptomatic bradycardia, congestive heart failure, or bundle branch block occurs. Transcutaneous or transvenous pacing may be necessary, particularly during an inferior MI.

2. Mobitz type 2 may progress to complete heart block and is an indication for pacemaker placement.

c. Third-degree AV block is treated with transcutaneous, transvenous, or epicardial pacing.

D. Supraventricular tachycardias originate at or above the bundle of His. The resulting QRS complexes are narrow (<120 milliseconds) except during aberrant conduction.

1. Atrial premature contractions (APCs) occur when ectopic foci in the atria fire before the next expected impulse from the sinus node. The P wave of an APC characteristically looks different from preceding P waves, and the PR interval may vary from normal. APCs may cause aberrant QRS complexes. If the AV node is still in a refractory period, an APC will not elicit a ventricular response. APCs are common, usually benign, and typically require no treatment.

2. Junctional or AV nodal rhythms are characterized by absent or abnormal P waves and normal QRS complexes. Although they may indicate ischemic cardiac disease, junctional rhythms are commonly seen in healthy individuals receiving inhalational anesthesia. In the patient whose cardiac output depends heavily on the contribution from atrial contraction, stroke volume and blood pressure may decline precipitously. Treatment may include the following:

a. Reduction of anesthetic depth.

b. Increasing intravascular volume.

c. Atropine in increments of 0.2 mg IV may convert a slow junctional rhythm to sinus rhythm, particularly if secondary to a vagal mechanism.

d. Paradoxically, β-blockers may be used cautiously (e.g., propranolol, 0.5 mg IV and metoprolol, 1 to 3 mg), especially with isorhythmic AV dissociation (independent atrial and ventricular rhythms that are similar in rate).

e. If the dysrhythmia is associated with hypotension, increasing the blood pressure with vasopressors (e.g., ephedrine or norepinephrine) may be required as a temporizing measure.

f. If necessary, atrial pacing may be instituted to restore atrial contraction.

3. Atrial fibrillation is an irregular rhythm with an atrial rate of 350 to 600 beats/minute and a variable ventricular response. It may be seen with myocardial ischemia, mitral valvular disease, hyperthyroidism, pulmonary embolism, excessive sympathetic stimulation, digitalis toxicity, after thoracic surgery, or when the heart has been manipulated. Treatment is based on the hemodynamic status.

a. Rapid ventricular rate with stable hemodynamics can be treated initially with β-adrenergic blockade, such as propranolol (0.5 mg increments IV), metoprolol (2.5- to 5-mg increments), esmolol (5 to 10 mg increments), or a calcium channel blocker such as verapamil (2.5- to 5-mg increments) or diltiazem (10 to 20 mg IV) (see Chapter 38). Amiodarone (150 mg IV) can be used to promote conversion back to sinus rhythm (anticoagulation prior to cardioversion is recommended in patients with atrial fibrillation for longer than 24 hours).

b. Rapid ventricular rate with unstable hemodynamics requires synchronized cardioversion (50 to 100 J if biphasic or 200 J if monophasic) (see Chapter 38).

4. Atrial flutter is usually a regular rhythm with an atrial rate of 250 to 350 beats/minute and a characteristic sawtooth ECG configuration. It is often seen with underlying heart disease (i.e., rheumatic heart disease and mitral stenosis). A 2:1 block will result in a rapid ventricular rate (usually 150 beats/minute). Treatment usually includes β-adrenergic, calcium channel blockade or synchronized cardioversion (see Chapter 38).

5. Paroxysmal supraventricular tachycardia is an abrupt onset tachydysrhythmia (atrial and ventricular rates of 150 to 250 beats/minute) with reentry usually through the AV node. This rhythm may be associated with Wolff-Parkinson-White [WPW] syndrome, thyrotoxicosis, or mitral valve prolapse. Patients without heart disease may develop this dysrhythmia due to stress, caffeine, or excess catecholamines. Treatment includes adenosine (6 to 18 mg IV, 3 mg if given centrally), Valsalva maneuvers, carotid sinus massage, or propranolol (1 to 2 mg IV). AV nodal blockers (calcium channel and β-blockers) are contraindicated for the treatment of atrial fibrillation or atrial flutter in patients with WPW syndrome as they selectively slow conduction through the AV node, which can lead to increased conduction through the accessory pathway and cause ventricular fibrillation. Synchronized cardioversion may be required for the hemodynamically unstable patient (also see Chapter 38).

1. Ventricular premature contractions (VPCs) occur when ectopic foci in the ventricle fire before the next expected impulse arrives. They are characterized by widened QRS (>120 milliseconds) complexes.
When coupled alternately with normal beats, ventricular bigeminy exists. VPCs are occasionally seen in healthy individuals. Under anesthesia, they frequently occur during states of catecholamine excess, hypoxia, or hypercarbia. They may also signify myocardial ischemia or infarction, digitalis toxicity, or hypokalemia. VPCs may require therapy when they are multifocal, occur in runs (>2 sequentially), increase in frequency (>10% of all ventricular depolarizations), or occur on or near the preceding T wave (R-on-T phenomenon); these situations may precede the development of ventricular tachycardia, ventricular fibrillation, and cardiac arrest. Treatment in an otherwise healthy individual may include deepening anesthesia and ensuring adequate oxygenation, ventilation while assessing for electrolyte abnormalities (especially potassium, and magnesium). Patients with coronary artery disease who continue to have ventricular irritability should have any ischemia treated. If the ectopy continues, then amiodarone (150 mg IV over 10 minutes followed by an infusion at 1 mg/minute for 6 hours then 0.5 mg/minute thereafter) may be considered. Refractory ventricular ectopy may require further treatment (see Chapter 38).

2. Ventricular tachycardia is a wide-complex tachydysrhythmia at a rate of 150 to 250 beats/minute. Hemodynamically unstable patients with a pulse should be treated as outlined in the ACLS guidelines with cardiopulmonary resuscitation and cardioversion (100 J if biphasic, or 200 J if monophasic; if unresponsive, may increase energy in a stepwise fashion). For stable patients the first-line treatment depends on whether the ventricular tachycardia is monomorphic or polymorphic. If polymorphic, treat as if unstable. In addition, the treatment may depend on the ejection fraction (see Chapter 38 for specific recommendations).

3. Ventricular fibrillation is chaotic ventricular activity resulting in ineffective ventricular contractions. Cardiopulmonary resuscitation and defibrillation are required (see Chapter 38 for specific recommendations).

4. Ventricular preexcitation. WPW syndrome is due to an accessory pathway connecting the atria and ventricle. The most common mechanism is characterized by antegrade conduction through the normal AV conduction system and retrograde conduction through the accessory pathway. Characteristic ECG findings include a short PR interval and a slurred “delta wave” at the upstroke of the QRS. Tachydysrhythmias are common. The treatment depends on whether the patient is hemodynamically stable (see Chapter 38). Unstable patients should receive synchronized cardioversion starting at 50 J (monophasic or biphasic). These patients are at high risk for ventricular fibrillation.

Hypoxemia occurs when oxygen delivery to the tissues is insufficient to meet metabolic demands.

a. Loss of the main pipeline supply with an empty reserve oxygen tank.

b. An oxygen flowmeter that is not turned to a sufficient flow.