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 the presence of dysrhythmias.

1. Contractility

   Most anesthetic agents, including inhalational agents, barbiturates, benzodiazepines, and etomidate (see Chapter 12) cause dose-dependent direct myocardial depression. Opiates are not direct myocardial depressants in usual clinical doses, although clinically significant bradycardia and hypotension may be observed owing to decreased sympathetic outflow. Although ketamine can cause a dose-dependent increase in sympathetic nervous system discharge, its direct myocardial depressant effects may be unmasked in patients with depleted endogenous catecholamines, myocardial depressants such as β-adrenergic antagonists, calcium channel blockers, and lidocaine.

   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).

2. Decreased SVR
   1. A decrease in SVR can be seen with many of the drugs administered during anesthesia.
      1. Isoflurane and, to a lesser extent, sevoflurane and desflurane produce a dose-dependent decrease in SVR.
      2. Opiates and propofol produce loss of vascular tone by reducing sympathetic nervous system outflow.
      3. Benzodiazepines may decrease SVR, particularly when administered at high doses in conjunction with opiates.
      4. Direct vasodilators (eg, nitroprusside, nitroglycerin, and hydralazine).
      5. α₁-Adrenergic blockers (eg, droperidol, chlorpromazine, phentolamine, and labetalol, prazosin, doxazosin).
      6. α₂-Adrenergic agonists (eg, clonidine and dexmedetomidine).
      7. Histamine-releasing medications (eg, d-tubocurarine, mivacurium, and morphine).
      8. Calcium channel blockers.
      9. Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers.
      10. Inodilators (eg, milrinone).
   2. Sympathetic blockade occurs during spinal and epidural anesthesia, particularly with blocks at higher dermatomes, leading to a reduction in SVR and/or preload.
   3. Sepsis causes release of vasoactive substances that mediate peripheral vasodilation.
   4. Vasoactive metabolites are released during bowel manipulation, aortic cross-clamp release, or tourniquet release.
   5. Allergic reactions (see Section XVIII).
   6. Profound hypoxia.
   7. Adrenal insufficiency (including iatrogenic causes).
3. Inadequate venous return (preload).
   1. Hypovolemia may be caused by blood loss, insensible evaporative losses, and preoperative deficits (eg, NPO (nothing by mouth) status, vomiting, diarrhea, nasogastric tube suction, enteric drains, and certain bowel preparations), or polyuria (eg, diuretic use, diabetes mellitus, diabetes insipidus, or postobstructive diuresis).

      Positive pressure variation: In patients undergoing positive-pressure ventilation, changes in cardiac output, and therefore 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 10 mm Hg in a paralyzed and mechanically ventilated patient.

   2. Caval compression may result from a gravid uterus, massive ascites, tumor, or 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:
      1. Sympathetic blockade (eg, ganglionic blockers or regional anesthesia).
      2. Direct vasodilators (eg, nitroglycerin).
      3. Histamine-releasing medications (eg, morphine, mivacurium).
      4. Medications that reduce sympathetic outflow (eg, propofol, inhalational agents, and opioids).
   4. Increased intrathoracic pressure will impair venous return. Possible causes include mechanical compression (eg, positioning, surgeon leaning on patient), 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 side of the heart.
      1. Tension pneumothorax leads to compression of the heart and great vessels. The resulting elevation in CVP decreases preload and gives rise to hypotension.
      2. Cardiac tamponade is a collection of fluid or clot in the pericardial space causing compression of the heart, resulting in decreased filling due to elevated intrapericardial pressures.
      3. Pulmonary embolism obstructs right ventricular ejection and in turn raises right atrial pressure, which can drastically reduce venous return.
      4. Intra-abdominal hypertension causes increased intrathoracic pressure, which then compresses the heart and raises the CVP. Thus the CVP can be elevated while the heart is severely underfilled.
4. Dysrhythmias (also see Section III)
   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.
5. Treatment of hypotension should be directed toward correcting the underlying cause. Depending on the etiology, appropriate maneuvers include:
   1. Decreasing anesthetic depth.
   2. Volume expansion (eg, administration of blood products, colloids, or crystalloids).
   3. Vasopressor support to increase vascular resistance or decrease venous capacitance (eg, phenylephrine and vasopressin if acidemic) and increase stroke volume (eg, 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 (eg, left uterine displacement for a pregnant patient), surgically relieving intra-abdominal hypertension, or surgically removing a massive pulmonary embolism (PE).
   5. Antidysrhythmic (see Section III) may include β-blockers, calcium channel blockers, and amiodarone.
   6. Inotropic support (eg, 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 (eg, transthoracic echocardiography (TTE)) and the placement of invasive monitors (eg, arterial line, central venous catheter, pulmonary artery catheter, transesophageal echocardiography (TEE)) to facilitate the identification of decreased cardiac output or SVR.