Autonomic Nervous System, IV Fluids
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Questions and Answers

What is primarily controlled by the autonomic nervous system?

  • Sensory perception
  • Conscious thought processes
  • Involuntary physiological actions (correct)
  • Voluntary muscle movements

    • Which component of the ANS is involved in the 'fight-or-flight' response?

  • Sympathetic nervous system (correct)
  • Central nervous system
  • Enteric nervous system
  • Parasympathetic nervous system

    • What does the term 'parasympathetic' signify in relation to its meaning?

  • Control of voluntary actions
  • Uncoordinated organ system interactions
  • Functioning independently of the CNS
  • Near or against sympathetic actions (correct)

    • Where do preganglionic sympathetic neurons originate in the spinal cord?

    <p>From the intermediolateral columns</p> Signup and view all the answers

    What type of ganglia is paired and located lateral to the vertebral column?

    <p>Paravertebral sympathetic ganglia</p> Signup and view all the answers

    What is the primary function of the adrenal medulla concerning catecholamines?

    <p>To secrete catecholamines directly into the venous blood stream.</p> Signup and view all the answers

    Which neurotransmitter is released by postganglionic adrenergic neurons at their target organs?

    <p>Norepinephrine</p> Signup and view all the answers

    What percentage of parasympathetic nervous system traffic is accommodated by the vagus nerve?

    <p>75%</p> Signup and view all the answers

    Which of the following adrenergic receptors inhibits the release of norepinephrine?

    <p>Alpha-2 (α2)</p> Signup and view all the answers

    Which of the following is a naturally occurring catecholamine?

    <p>Dopamine</p> Signup and view all the answers

    What is a major reason for measuring the metabolites of epinephrine and norepinephrine when diagnosing pheochromocytoma?

    <p>Their half-life is significantly longer than catecholamines.</p> Signup and view all the answers

    What severe effects might result from excessive accumulation of acetylcholine due to AChE inhibition?

    <p>Muscular paralysis and blindness.</p> Signup and view all the answers

    Which statement is true regarding the effects of β2 antagonists?

    <p>They typically cause peripheral vasoconstriction and bronchoconstriction.</p> Signup and view all the answers

    What is the role of atropine in treating cholinergic crisis?

    <p>Antagonizes muscarinic receptors in some organs.</p> Signup and view all the answers

    How does β-blockade affect the surgical stress response?

    <p>It may attenuate the stress response but not protect from harm.</p> Signup and view all the answers

    What is a primary risk associated with abruptly stopping clonidine before surgery?

    <p>Rebound hypertension</p> Signup and view all the answers

    Which muscarinic antagonist is primarily used to minimize side effects when reversing neuromuscular blockade?

    <p>Glycopyrrolate</p> Signup and view all the answers

    What condition is characterized by exaggerated sympathetic responses to stimuli below the level of a spinal cord lesion?

    <p>Autonomic dysreflexia</p> Signup and view all the answers

    How is pheochromocytoma primarily diagnosed?

    <p>Computed tomography (CT) scan</p> Signup and view all the answers

    Which sympathetic response occurs in patients experiencing hemorrhage?

    <p>Increased sympathetic tone</p> Signup and view all the answers

    What is the primary physiological effect of increased sympathetic tone on the arteries?

    <p>Increased systemic vascular resistance</p> Signup and view all the answers

    Which of the following best describes the function of the heart?

    <p>To generate a pressure gradient for blood delivery</p> Signup and view all the answers

    In individuals with diminished physiological reserve, what is a significant factor affecting their response to blood loss?

    <p>Presence of medications that blunt physiological response</p> Signup and view all the answers

    What factor primarily regulates body water and tonicity in the kidneys?

    <p>Antidiuretic hormone (ADH)</p> Signup and view all the answers

    Which statement about total body water distribution is correct?

    <p>Total body water accounts for about 60% of body weight</p> Signup and view all the answers

    Which of the following conditions is a direct stimulant for the release of ADH?

    <p>Hypovolemia</p> Signup and view all the answers

    What is the primary reason that ADH can be secreted to maintain volume even if it affects osmolarity?

    <p>ADH secretion is prioritized in conditions of volume deficiency.</p> Signup and view all the answers

    Which factors can lead to diabetes insipidus (DI) due to vasopressin insensitivity?

    <p>Acquired conditions and hypercalcemia</p> Signup and view all the answers

    What is the primary symptom of hyponatremia caused by SIADH?

    <p>Altered mental status</p> Signup and view all the answers

    Which management approach should not be used in patients with severe symptomatic hyponatremia due to SIADH?

    <p>Normal saline infusion</p> Signup and view all the answers

    What is the primary consequence of stress-induced hyponatremia during critical illness or surgery?

    <p>Decreased urine output without hypovolemia</p> Signup and view all the answers

    What stimulates the juxtaglomerular cells to release renin?

    <p>Decreased blood pressure or hypovolemia</p> Signup and view all the answers

    What can be a common cause of hypovolemia in the perioperative period?

    <p>Blood loss during surgery</p> Signup and view all the answers

    What is often the result of over-resuscitation during surgery?

    <p>Increased risk of hypervolemia and complications</p> Signup and view all the answers

    What is the treatment approach for patients experiencing contraction alkalosis?

    <p>Volume resuscitation with high chloride solutions</p> Signup and view all the answers

    What is a potential benefit of using restrictive fluid maintenance during abdominal surgery?

    <p>Shorter length of hospital stay</p> Signup and view all the answers

    Why are isotonic or balanced salt solutions recommended over hypotonic solutions for patients in acute illness?

    <p>They minimize the risk of hyponatremia</p> Signup and view all the answers

    What is the effect of adding sodium bicarbonate to a crystalloid solution for patients with metabolic acidosis?

    <p>Produces an alkalotic solution</p> Signup and view all the answers

    What is one reason that manufacturers do not add bicarbonate directly to normal saline solutions?

    <p>It can lead to precipitation of calcium and magnesium</p> Signup and view all the answers

    What is the main concern with fluid management in patients undergoing thoracotomy?

    <p>Postoperative pulmonary edema</p> Signup and view all the answers

    What is the primary enzyme that metabolizes acetylcholine in the junctional cleft?

    <p>Acetylcholinesterase</p> Signup and view all the answers

    Which of the following side effects is commonly associated with excessive accumulation of acetylcholine?

    <p>Bronchoconstriction</p> Signup and view all the answers

    What is a potential consequence of abrupt withdrawal of β-blockers?

    <p>Receptor upregulation leading to hypertension</p> Signup and view all the answers

    Which treatment is primarily used for managing bradycardia during intraoperative β blockade?

    <p>Atropine</p> Signup and view all the answers

    What effect do β2 antagonists have on bronchial smooth muscle?

    <p>Bronchoconstriction</p> Signup and view all the answers

    What is the primary physiological response that occurs when the body experiences hypotension?

    <p>Facilitation of ADH release</p> Signup and view all the answers

    Which condition is characterized by the renal response to ADH being impaired?

    <p>Nephrogenic diabetes insipidus</p> Signup and view all the answers

    Which of the following best describes a key feature in managing patients with SIADH?

    <p>Water restriction as the primary therapy</p> Signup and view all the answers

    What is one of the main determinants for the release of ADH aside from osmolarity?

    <p>Sympathetic nerve activity</p> Signup and view all the answers

    What clinical test is commonly used to confirm the diagnosis of diabetes insipidus?

    <p>Fluid restriction test</p> Signup and view all the answers

    Which statement best describes the primary function of the autonomic nervous system?

    <p>It controls physiological actions unconsciously.</p> Signup and view all the answers

    What physiological state is associated with the predominance of the parasympathetic nervous system?

    <p>Rest-and-digest state.</p> Signup and view all the answers

    Which component of the ANS is primarily responsible for regulating GI tract function?

    <p>Enteric nervous system.</p> Signup and view all the answers

    What is a defining characteristic of the sympathetic nervous system compared to the parasympathetic nervous system?

    <p>Widespread effects throughout the body.</p> Signup and view all the answers

    What is the origin of the term 'sympathetic' in the context of the autonomic nervous system?

    <p>It comes from the Greek word meaning 'to act together'.</p> Signup and view all the answers

    What is the primary neurotransmitter released by postganglionic neurons in the sympathetic nervous system?

    <p>Norepinephrine</p> Signup and view all the answers

    What is the main effector role of the celiac plexus?

    <p>Providing sympathetic innervation to abdominal organs</p> Signup and view all the answers

    Which receptor is primarily involved in the vasodilation of arteries in skeletal muscle?

    <p>Beta-2 (β2) receptor</p> Signup and view all the answers

    Where do preganglionic parasympathetic neurons predominantly originate from?

    <p>Sacral segments and cranial nerves</p> Signup and view all the answers

    What are the natural catecholamines produced in the body?

    <p>Epinephrine, norepinephrine, and dopamine</p> Signup and view all the answers

    What is the primary reason glycopyrrolate is favored over atropine in the operating room for reversing neuromuscular blockade?

    <p>Glycopyrrolate does not cross the blood-brain barrier.</p> Signup and view all the answers

    Which potential risk is associated with autonomic dysfunction during surgery?

    <p>Severe hypotension and aspiration from gastroparesis.</p> Signup and view all the answers

    How does spinal cord injury at T6 or above affect the autonomic nervous system?

    <p>It may cause autonomic dysreflexia and exaggerated sympathetic responses.</p> Signup and view all the answers

    What are the primary symptoms associated with a pheochromocytoma?

    <p>Paroxysms of hypertension, headache, and diaphoresis.</p> Signup and view all the answers

    What factor primarily leads to increased sympathetic tone in the setting of hemorrhage?

    <p>Decrease in blood pressure.</p> Signup and view all the answers

    What primarily facilitates venous return during increased sympathetic tone?

    <p>Decreased venous compliance</p> Signup and view all the answers

    Which lung volume is defined as the total amount of air that can be exhaled after a maximal inhalation?

    <p>Vital capacity (VC)</p> Signup and view all the answers

    What is the primary consequence of aging related to physiological reserve in response to blood loss?

    <p>Decreased ability to tolerate blood loss</p> Signup and view all the answers

    Which factor does NOT influence the net filtration across capillaries according to the revised Sterling’s principle?

    <p>Interstitial carbon dioxide level</p> Signup and view all the answers

    How is serum osmolarity typically calculated for a rough estimate?

    <p>Doubling the sodium concentration</p> Signup and view all the answers

    What physiological response facilitates the release of ADH during stress-induced hyponatremia?

    <p>Elevated sympathetic tone</p> Signup and view all the answers

    What are the consequences of hypovolemia during the perioperative period?

    <p>Shock physiology</p> Signup and view all the answers

    Which factors primarily stimulate the release of aldosterone?

    <p>Decreased renal blood flow and hyperkalemia</p> Signup and view all the answers

    What is a common misperception regarding urine output during critical illness?

    <p>Urine output can be misleading in assessing total body fluid status</p> Signup and view all the answers

    What is the main treatment strategy for patients with contraction alkalosis?

    <p>Chloride and volume resuscitation</p> Signup and view all the answers

    What is a significant benefit of using restrictive fluid maintenance during abdominal surgery?

    <p>Shorter length of stay in the hospital</p> Signup and view all the answers

    Why are isotonic or balanced salt solutions preferred over hypotonic solutions for maintenance fluids in acutely ill patients?

    <p>They minimize the risk of hyponatremia</p> Signup and view all the answers

    What effect does the addition of sodium bicarbonate to a crystalloid solution have for patients with metabolic acidosis?

    <p>Increases the pH of the solution</p> Signup and view all the answers

    Which component in balanced salt solutions helps maintain a physiological pH after their administration?

    <p>Lactate metabolism by the liver</p> Signup and view all the answers

    What is the primary reason manufacturers do not include bicarbonate in normal saline solutions?

    <p>Bicarbonate can lead to the precipitation of calcium and magnesium</p> Signup and view all the answers

    Which of the following metabolites is primarily associated with norepinephrine?

    <p>Normetanephrine</p> Signup and view all the answers

    What effect does β2 antagonism have on the body's physiological responses?

    <p>Bronchospasm</p> Signup and view all the answers

    What is a potential complication of β-blocker therapy during surgery?

    <p>Hyperkalemia</p> Signup and view all the answers

    In treating cholinergic crisis, which is the primary role of atropine?

    <p>Block muscarinic receptors</p> Signup and view all the answers

    Which treatment option is considered for refractory bradycardia during intraoperative β blockade?

    <p>Isoproterenol infusion</p> Signup and view all the answers

    What distinguishes the enteric nervous system (ENS) from the sympathetic and parasympathetic nervous systems?

    <p>It governs the function of the GI tract and can operate independently of the CNS.</p> Signup and view all the answers

    Which of the following statements correctly describes the effects of the sympathetic nervous system (SNS)?

    <p>The SNS mobilizes energy resources to prepare for fight-or-flight responses.</p> Signup and view all the answers

    What anatomical feature is unique to the prevertebral sympathetic ganglia?

    <p>They are unpaired and located anterior to the vertebral column.</p> Signup and view all the answers

    Which component of the autonomic nervous system is primarily responsible for opposing the sympathetic nervous system's effects?

    <p>Parasympathetic nervous system</p> Signup and view all the answers

    The term 'sympathetic' in the sympathetic nervous system originates from which concept?

    <p>A physiological 'sympathy' facilitating interactions among organ systems.</p> Signup and view all the answers

    What condition may result from both impaired release of ADH and renal resistance to ADH?

    <p>Diabetes Insipidus</p> Signup and view all the answers

    Which physiological state would inhibit the release of ADH?

    <p>Hypoosmolarity</p> Signup and view all the answers

    Which factor does NOT contribute to the synthesis of ADH?

    <p>Renal resistance to ADH</p> Signup and view all the answers

    What is a common clinical testing method for confirming Diabetes Insipidus?

    <p>Cautious fluid restriction</p> Signup and view all the answers

    Which treatment strategy may respond well in cases of incomplete diabetes insipidus?

    <p>Thiazide diuretics</p> Signup and view all the answers

    Which of the following statements about preganglionic sympathetic neurons is true?

    <p>They may synapse with multiple ganglia.</p> Signup and view all the answers

    What anatomical structure provides sympathetic innervation to the abdominal organs?

    <p>Celiac plexus</p> Signup and view all the answers

    Which class of receptors are primarily involved in the response to catecholamine release from the adrenal medulla?

    <p>Beta-adrenergic receptors</p> Signup and view all the answers

    What is a key feature of the autonomic nervous system's parasympathetic division?

    <p>Muscarinic receptors respond to acetylcholine at target organs.</p> Signup and view all the answers

    Which statement accurately describes the metabolic pathways of catecholamines?

    <p>Epinephrine is synthesized from norepinephrine in the adrenal medulla.</p> Signup and view all the answers

    What effect do norepinephrine and epinephrine primarily have on the venous system?

    <p>Decrease venous compliance to facilitate venous return</p> Signup and view all the answers

    Which patient population is more likely to experience diminished physiological reserve when responding to blood loss?

    <p>Older patients with conditions such as atherosclerosis</p> Signup and view all the answers

    What primarily regulates the ability of kidneys to manage body water and tonicity?

    <p>Antidiuretic hormone (ADH) acting on renal structures</p> Signup and view all the answers

    How does the concept of Sterling's principle evolve with the inclusion of the endothelial glycocalyx?

    <p>It reflects continuous filtration across the entire capillary length</p> Signup and view all the answers

    What characterizes the distribution of total body water in a typical adult?

    <p>40% intracellular, 20% extracellular, and 60% total body water</p> Signup and view all the answers

    How can acute withdrawal of clonidine affect a patient undergoing surgery?

    <p>It can lead to rebound hypertension.</p> Signup and view all the answers

    What physiological condition can result from a pheochromocytoma related to catecholamine secretion?

    <p>Exaggerated hypertensive episodes.</p> Signup and view all the answers

    What mechanism allows glycopyrrolate to effectively reduce side effects when reversing neuromuscular blockade?

    <p>It is a quaternary amine and does not cross the blood-brain barrier.</p> Signup and view all the answers

    What is a potential complication for patients with high spinal cord injuries concerning their autonomic nervous system?

    <p>Autonomic dysreflexia due to exaggerated sympathetic responses.</p> Signup and view all the answers

    What is the primary diagnostic method for confirming a pheochromocytoma?

    <p>Plasma levels of normetanephrine and metanephrine.</p> Signup and view all the answers

    What mechanism primarily causes stress-induced hyponatremia during surgical procedures?

    <p>Increased sympathetic tone leading to ADH release</p> Signup and view all the answers

    Which electrolyte imbalance is a stimulus for aldosterone release aside from low blood pressure?

    <p>Hyperkalemia</p> Signup and view all the answers

    Why is urine output considered a poor indicator of volume status during critical illness?

    <p>ADH release can lead to water retention, maintaining low urine output despite euvolemia</p> Signup and view all the answers

    What is the primary physiological consequence of hypovolemia during surgical procedures?

    <p>Decreased cardiac output and tissue perfusion</p> Signup and view all the answers

    What is a common cause of contraction alkalosis in surgical patients?

    <p>Diuretic use combined with chloride restriction</p> Signup and view all the answers

    What is the primary advantage of using restrictive fluid maintenance during abdominal surgery?

    <p>Better postoperative bowel function and wound healing</p> Signup and view all the answers

    Why should hypotonic saline be avoided in hospitalized patients with acute illnesses?

    <p>It can predispose patients to hyponatremia due to elevated ADH levels</p> Signup and view all the answers

    What is one reason that balanced salt solutions like Lactated Ringer's are preferred over normal saline?

    <p>They maintain a more physiological pH</p> Signup and view all the answers

    What effect does adding sodium bicarbonate to a crystalloid solution have for patients with metabolic acidosis?

    <p>Increases the osmolarity of the solution</p> Signup and view all the answers

    Why is sodium bicarbonate not added directly to normal saline by manufacturers?

    <p>It leads to precipitation of calcium and magnesium</p> Signup and view all the answers

    Study Notes

    Autonomic Nervous System

    • The autonomic nervous system (ANS) is a network of nerves and ganglia that involuntarily control physiological actions like homeostasis.
    • The ANS innervates various systems and can influence metabolism and thermal regulation.
    • The ANS consists of the sympathetic nervous system (SNS), parasympathetic nervous system (PNS), and enteric nervous system (ENS).
    • The ENS manages the GI tract and is independent of the CNS.
    • The SNS has widespread effects while the PNS has more localized, discrete effects.
    • SNS and PNS generally have opposing effects on most organs. The PNS predominates at rest ('rest-and-digest'), while the SNS predominates during stress ('fight-or-flight').

    Sympathetic Nervous System Anatomy

    • Preganglionic sympathetic neurons originate from the spinal cord (T1-L2).
    • Myelinated fibers travel through the sympathetic chain and synapse with ganglia:
      • Paravertebral sympathetic ganglia are a chain of paired ganglia, lateral to the vertebral column, extending from the skull to the coccyx, forming the sympathetic trunk.
      • Prevertebral sympathetic ganglia are unpaired ganglia located anterior to the vertebral column.
      • Adrenal medulla is a modified ganglia within the adrenal gland. It directly secretes catecholamines into the bloodstream.
    • Preganglionic sympathetic fibers can ascend or descend the sympathetic chain, and a single fiber can synapse with multiple ganglia.
    • Most preganglionic sympathetic fibers synapse with paravertebral ganglia, while others synapse with prevertebral ganglia or the adrenal medulla.
    • Preganglionic sympathetic fibers release acetylcholine, stimulating nicotinic cholinergic postganglionic neurons (or chromaffin cells).
    • Postganglionic neurons release norepinephrine (except for sweat glands, which release acetylcholine).

    Sympathetic Ganglia Targets

    • Stellate ganglia are paired paravertebral ganglia, located at the level of C7, providing sympathetic innervation to the head, neck, and upper extremities.
    • Celiac plexus is a collection of prevertebral sympathetic ganglia located anterior to the aorta, supplying sensory and sympathetic outflow to the stomach, liver, spleen, pancreas, kidney, and the GI tract up to the splenic flexure.

    Parasympathetic Nervous System Anatomy

    • Preganglionic parasympathetic neurons originate from cranial nerves III, VII, IX, and X, and sacral segments 2-4.
    • The vagus nerve carries approximately 75% of PNS traffic.
    • Preganglionic parasympathetic neurons synapse with postganglionic neurons close to the target organ, facilitating fine, discrete physiological effects.
    • Both preganglionic and postganglionic parasympathetic neurons release acetylcholine, interacting with either nicotinic or muscarinic receptors.

    Adrenergic Receptors

    • Adrenergic receptors are α1, α2, β1, and β2.
    • α1, β1, and β2 receptors are postsynaptic, stimulated by norepinephrine.
    • α2 receptors are presynaptic, also stimulated by norepinephrine.
    • α2 receptors inhibit presynaptic release of norepinephrine.

    Catecholamines

    • Catecholamines are monoamines stimulating adrenergic nerve terminals.
    • Naturally occurring catecholamines are norepinephrine, epinephrine, and dopamine.
    • Synthetic catecholamines are dobutamine and isoproterenol.

    Catecholamine Synthesis

    • Tyrosine is converted to dopamine by two enzymatic reactions: hydroxylation by tyrosine hydroxylase to L-DOPA and decarboxylation by aromatic l-amino acid decarboxylase to dopamine.
    • Dopamine is transported into storage vesicles and hydroxylated by dopamine β-hydroxylase to norepinephrine.
    • Epinephrine is synthesized from norepinephrine in the adrenal medulla through methylation by phenylethanolamine N-methyltransferase.

    Catecholamine Metabolism

    • Norepinephrine is primarily removed by reuptake into the presynaptic nerve terminal, with a small amount entering the circulation and undergoing metabolism.
    • Catecholamines are metabolized by monoamine oxidase and catecholamine O-methyltransferase in the blood, liver, and kidney.
    • The important metabolites of epinephrine and norepinephrine are metanephrine and normetanephrine, respectively.

    Significance of Metabolites

    • The half-life of catecholamines is very short (t1/2 ≈ 2 minutes), making direct measurement difficult.
    • Catecholamine metabolites, metanephrine and normetanephrine, have a longer half-life (t1/2 ≈ 1–2 hours) and are used to diagnose pheochromocytoma.

    Acetylcholine Metabolism

    • Acetylcholine (ACh) is metabolized to choline and acetate by acetylcholinesterase (AChE), an enzyme located in the junctional cleft.

    Effects of ACh Accumulation

    • Inhibition of AChE leads to ACh accumulation, causing side effects like bradycardia, salivation, lacrimation, urination, defecation, and emesis.
    • Excessive accumulation can result in cholinergic crisis, causing severe bradycardia, bronchoconstriction, blindness, muscular paralysis, and other severe effects.
    • Cholinergic crisis can be caused by pesticides or chemical warfare agents.

    Cholinergic Crisis Treatment

    • Cholinergic crisis is treated with atropine and intubation for respiratory support.

    β-Adrenergic Antagonists

    • β-adrenergic antagonists (β blockers) are antagonists at β1 and β2 receptors, commonly used for hypertension, angina, and dysrhythmias.
    • Perioperative β blockade is essential in patients with coronary artery disease, reducing death risk after myocardial infarction.

    Mechanism and Side Effects of β-Blockers

    • β1 and β2 antagonism decreases adenylate cyclase activation, reducing cyclic adenosine monophosphate (cAMP) production.
    • β blockers can be cardioselective (β1-selective) or noncardioselective.
    • β1 blockade lowers heart rate, contractility, cardiac output, and myocardial oxygen requirement.
    • β1 blockers inhibit renin secretion, reducing fluid retention and angiotensin II.
    • Abrupt withdrawal is not recommended due to receptor upregulation, which can lead to hypertension, tachycardia, and myocardial ischemia.
    • β blockers can cause hyperkalemia.
    • They can mask hypoglycemia signs like tachycardia and tremor.

    Effects of β2 Antagonism

    • β2 receptors are located on vascular and bronchial smooth muscle.
    • β2 blockade causes peripheral vasoconstriction, bronchoconstriction, and inhibits insulin release and glycogenolysis.
    • Selective β1 blockers are preferred in patients with peripheral vascular disease, chronic obstructive pulmonary disease, or reactive airway disease.

    β Blockade and Surgical Stress

    • β antagonism can attenuate the adrenergic response to perioperative stimuli like intubation or incision.
    • The adrenergic response to surgical stress is best managed through a combination of anesthetic agents, opioids, and β antagonists.

    Management of β Blockade Complications

    • Bradycardia and heart block respond to atropine or glycopyrrolate, while refractory cases may require β1-agonism with epinephrine, dobutamine, or isoproterenol.
    • Other treatment options include glucagon, calcium, insulin and glucose, and lipid emulsion therapy.

    α2 Agonists

    • α2 agonists inhibit adenylate cyclase and decrease cAMP production, reducing sympathetic outflow from the CNS.
    • Dexmedetomidine is the most common α2 agonist in the perioperative setting, producing sedation, analgesia, lowers anesthetic requirements, and reduces heart rate and blood pressure.
    • Side effects include bradycardia, which can be treated with glycopyrrolate.
    • Clonidine is another α2 agonist used for hypertension. It can cause rebound hypertension if stopped abruptly before surgery.

    Muscarinic Antagonists and Neuromuscular Blockade

    • Nondepolarizing muscle relaxants can be reversed with AChE inhibitors, which increase ACh at the neuromuscular junction (nicotinic receptor).
    • AChE inhibitors also increase ACh at the parasympathetic innervated organs (muscarinic receptor), causing bradycardia, defecation, secretions, and bronchospasm.
    • Muscarinic antagonists (e.g., glycopyrrolate) are coadministered with AChE inhibitors to minimize these side effects.

    Glycopyrrolate

    • Glycopyrrolate is commonly used to reverse neuromuscular blockade.
    • It is a quaternary amine, a polar molecule that does not readily cross the blood-brain barrier, minimizing CNS anticholinergic effects.

    Autonomic Dysfunction

    • Patients with autonomic dysfunction or dysautonomia are at risk of intraoperative hypotension and aspiration due to gastroparesis.
    • Risk factors include diabetes mellitus and chronic alcohol abuse.

    Spinal Cord Injury

    • Spinal cord injury can cause ANS problems based on the site, extent, and timing of the lesion.
    • Autonomic reflexes normally inhibited by supraspinal feedback are lost after a high (T6 or above) spinal cord injury.
    • Spinal shock, with vasodilation and compensatory tachycardia, can occur initially.
    • Hypotension with bradycardia can occur as the injury becomes chronic.
    • Upregulation of adrenergic receptors can make patients sensitive to vasopressors.
    • Pressure stimuli below the lesion can cause autonomic dysreflexia (increased blood pressure and reflexive decline in heart rate), which can be managed with vasodilators or anesthetic deepening.
    • Regional anesthesia is recommended to blunt the exaggerated sympathetic response.

    Pheochromocytoma

    • Pheochromocytoma is a catecholamine-secreting tumor, usually intraadrenal but may be extraadrenal.
    • Symptoms include paroxysmal hypertension, headache, palpitations, flushing, and diaphoresis.
    • Diagnosis is confirmed by detecting elevated levels of catecholamine metabolites (metanephrine and normetanephrine) in the plasma or 24-hour urine.

    Key Points

    • Sympathetic nerves originate from T1–L2, and parasympathetic nerves from cranial nerves III, VII, IX, X, and S2–S4.
    • The stellate ganglion supplies the upper extremity, while the celiac plexus supplies abdominal organs.
    • Patients on β-blockers should continue them perioperatively to avoid receptor upregulation.
    • High spinal cord injuries (T6 and above) pose a risk for autonomic dysreflexia.
    • Pheochromocytoma is a catecholamine-secreting tumor, diagnosed by elevated metanephrine and normetanephrine levels.

    Hemorrhage and Sympathetic Tone

    • Increased sympathetic tone in hemorrhage triggers norepinephrine and epinephrine release.
    • These hormones stimulate α1 adrenergic receptors on arterioles, increasing systemic vascular resistance (SVR) and preserving blood pressure.
    • They also stimulate α1 adrenergic receptors on veins, decreasing venous compliance and improving venous return.
    • Additionally, these catecholamines elevate heart rate and contractility, maintaining normal cardiac output.
    • Younger, healthy patients have greater physiological reserve, tolerating larger blood loss before vital signs become abnormal.
    • Older patients have diminished reserve due to atherosclerosis, decreased cardiac contractility, and medications like β-blockers that dampen their response.

    The Heart and its Function

    • The heart is a muscular organ responsible for pumping blood throughout the body.
    • It consists of four chambers: the right and left atria, and the right and left ventricles.
    • Each chamber is separated by one-way valves that regulate pressure.

    Lung Volumes and Capacities

    • Tidal volume (TV): Volume of air inhaled and exhaled during normal breathing.
    • Expiratory reserve volume (ERV): Maximum amount of air exhaled from rest.
    • Residual volume (RV): Air remaining in the lungs after a maximal exhale.
    • Functional residual capacity (FRC): ERV + RV.
    • Inspiratory reserve volume (IRV): Maximum amount of air inhaled beyond a normal TV.
    • Inspiratory capacity (IC): IRV + TV.
    • Vital capacity (VC): IRV + TV + ERV.
    • Total lung capacity (TLC): IRV + TV + ERV + RV.

    Body Water Compartments

    • Total body water comprises approximately 60% of body weight.
    • Intracellular fluid (ICF) constitutes about 40%.
    • Extracellular fluid (ECF) makes up the remaining 20%.
    • ECF is further divided into interstitial fluid (15%) and plasma volume (5%).

    Fluid Dynamics: Plasma and Endothelial Glycocalyx

    • Sterling’s principle describes filtration between the intravascular and interstitial space.
    • However, the endothelial glycocalyx plays an important role in fluid transfer.
    • This glycocalyx influences filtration throughout the capillary bed, while reabsorption from the interstitial space occurs.
    • Net filtration is regulated by the glycocalyx, endothelial basement membrane, and extracellular matrix.

    Serum Osmolarity

    • Normal serum osmolarity ranges between 285 and 305 mOsm/L.
    • It can roughly be estimated by doubling the sodium concentration.
    • A more accurate estimate uses the following equation:
    • United States Customary System (imperial system):
      • Osmolarity = 2(Sodium (mEq/L)) + Glucose (mg/dL)/18 + BUN (mg/dL)/2.8
    • International Systems of Units (metric system):
      • Osmolarity = 2(Sodium (mmol/L)) + Glucose (mmol/L) + BUN (mmol/L)
    • Osmolality (mOsm/kg) is practically equivalent to osmolarity, because 1 L of water = 1 kg of water.

    Regulation of Body Water and Tonicity

    • Antidiuretic hormone (ADH), also known as vasopressin, is crucial for regulating body water and tonicity.
    • ADH is released from the posterior pituitary in response to stimuli:
      • Hypothalamic osmoreceptors: detect hyperosmolarity.
      • Hypothalamic thirst center neurons: regulate thirst in response to hyperosmolarity.
      • Aortic baroreceptors: respond to hypotension.
      • Left atrial stretch receptors: respond to hypovolemia.
      • Increased sympathetic tone: caused by stress, surgery, or critical illness.
    • Hypovolemia and hypotension take precedence over osmolarity, meaning ADH may be secreted to maintain volume even at the expense of osmolarity.

    ADH Synthesis

    • ADH is synthesized in the supraoptic and paraventricular nuclei of the hypothalamus.
    • It travels down the pituitary stalk stored in secretory granules to the posterior pituitary.
    • ADH-producing neurons receive input from osmoreceptors and baroreceptors.

    ADH Release Conditions

    • Stimulate ADH Release:
      • Normal states: hyperosmolarity, hypovolemia, upright position, β-adrenergic stimulation, pain & emotional stress, cholinergic stimulation.
      • Abnormal states: hemorrhagic shock, hyperthermia, increased intracranial pressure, positive airway pressure, metabolic and respiratory acidosis.
      • Medications: morphine, nicotine, barbiturates, tricyclic antidepressants, chlorpropamide.
    • Inhibit ADH Release:
      • Normal states: hypoosmolarity, hypervolemia, supine position, α-adrenergic stimulation.
      • Medications: ethanol, atropine, phenytoin, glucocorticoids, chlorpromazine.

    Diabetes Insipidus (DI)

    • DI arises from impaired ADH release (neurogenic DI) or renal resistance to ADH (nephrogenic DI).
    • Characterized by large volumes of dilute urine, leading to dehydration, hypernatremia, and serum hyperosmolarity.
    • Diagnosis involves cautious fluid restriction, monitoring urine output and concentration, and plasma ADH measurements.
    • IV desmopressin (DDAVP) helps differentiate nephrogenic from neurogenic DI.

    Causes of DI

    • Vasopressin Deficiency (Neurogenic DI):
      • Familial (autosomal-dominant)
      • Acquired: idiopathic, craniofacial & basilar skull fractures, pituitary tumors/lymphoma/metastasis, granuloma (sarcoidosis, histiocytosis), CNS infections, Sheehan syndrome, hypoxic brain injury, brain herniation or death, pituitary surgery.
    • Vasopressin Insensitivity (Nephrogenic DI):
      • Familial (X-linked recessive)
      • Acquired: pyelonephritis, postrenal obstruction, sickle cell, amyloidosis, hypokalemia/hypercalcemia, sarcoidosis, lithium.

    Central DI Management

    • Available ADH preparations include DDAVP (2-4 mcg IV every 2-4 hours) or intravenous vasopressin (titrated to urine output ≤ 2.4 units/h).
    • Hypotonic maintenance fluids like dextrose 5% replace free water deficit. Avoid isotonic fluids like NS, as they can increase serum osmolarity.
    • Incomplete DI might respond to thiazide diuretics or chlorpropamide.
    • Frequent plasma and urine osmolarity measurements, along with urine output monitoring, are often necessary.

    Syndrome of Inappropriate ADH (SIADH)

    • SIADH involves nonosmotic ADH release, leading to serum hypotonicity due to water retention.
    • Diagnosis requires three criteria:
      • Euvolemia or hypervolemia.
      • Inappropriately concentrated urine (urine osmolarity > 100 mOsm/kg)
      • Normal renal, cardiac, hepatic, adrenal, and thyroid function.

    Managing SIADH

    • Primary therapy is water restriction, usually sufficient for asymptomatic hyponatremia.
    • Demeclocycline or vaptans, such as tolvaptan, may be needed for chronic SIADH.
    • Severe symptomatic hyponatremia requires intensive care and hypertonic saline.
    • Hyponatremia primarily presents as altered mental status due to cerebral edema and increased intracranial pressure (ICP).
    • Isotonic saline is not the solution: it can worsen hyponatremia by contributing to free water retention.

    SIADH-Associated Disorders

    • Central nervous system events: acute intracranial hypertension, trauma, tumors, meningitis, subarachnoid hemorrhage.
    • Pulmonary causes: tuberculosis, pneumonia, asthma, bronchiectasis, hypoxemia, hypercarbia, positive-pressure ventilation.
    • Malignancies: may produce ADH-like compounds.
    • Adrenal insufficiency and hypothyroidism.

    Stress-Induced Hyponatremia

    • Stressful situations like surgery and critical illness increase sympathetic tone, triggering ADH release and activating the renin-angiotensin-aldosterone system.
    • This leads to free water reabsorption and decreased urine output despite normal volume status.
    • Mild dilutional hyponatremia from this ADH release is termed stress-induced hyponatremia.
    • Urine output alone is a poor indicator of intraoperative volume status.

    Aldosterone

    • Aldosterone regulates sodium excretion, primarily controlled by the renin-angiotensin-aldosterone system.
    • Decreased renal or systemic arterial blood pressure, hypovolemia, and/or hyponatremia stimulate renin release from the juxtaglomerular cells of the kidney.
    • Renin converts angiotensinogen to angiotensin I, which is then converted to angiotensin II by angiotensin-converting enzyme (ACE) in the lung.
    • Angiotensin II stimulates the zona glomerulosa of the adrenal cortex to release aldosterone.
    • Aldosterone acts on the distal renal tubules and cortical collecting ducts, reabsorbing three sodium ions for every two potassium ions excreted, leading to net fluid retention.
    • Additional stimuli for aldosterone release include hyperkalemia, increased adrenocorticotropic hormone levels, and increased sympathetic tone.

    Perioperative Fluid Status Derangements

    • Preoperative Hypovolemia:
      • Bowel prep.
      • Active blood loss.
      • Inflammatory processes: sepsis, pancreatitis, small bowel obstruction.
      • Fasting for 10+ hours before surgery does not usually contribute significantly.
    • Intraoperative Factors:
      • Anesthetic medications: can cause vasodilation and hypotension.
      • Procedures: like spinal anesthesia, can induce vasodilation.
      • Blood loss (procedure-related).
      • Evaporative losses.
      • Third spacing.

    Consequences of Intraoperative Hypovolemia/Hypervolemia

    • Hypovolemia can decrease CO and tissue perfusion, potentially leading to shock.
    • Hypervolemia can contribute to:
      • Pulmonary edema.
      • Bowel edema.
      • Wound edema.
      • Dilution of coagulation factors, exacerbating blood loss.
    • Optimal volume resuscitation is crucial—avoid under- or overresuscitation.

    Contraction Alkalosis

    • Contraction alkalosis, or chloride depletion alkalosis, occurs with hypovolemia and hypochloremia.
    • Common examples include patients on diuretics (hypovolemia) with salt restriction (hypochloremia), or those with upper gastrointestinal losses (vomiting, nasogastric suction).
    • Bicarbonate is preferentially reabsorbed due to chloride depletion, maintaining electroneutrality.
    • Aldosterone-mediated renal hydrogen secretion also contributes.
    • Treatment requires both chloride and volume resuscitation.

    Fluid Administration During Surgery

    • Overresuscitation and excessive fluid balances increase the risk of hypervolemia and complications.
    • Restrictive fluid maintenance (3-5 mL/kg/h) during abdominal surgery has shown better outcomes compared to liberal resuscitation.
    • Fluid restriction is especially important with thoracotomy and lung resections to prevent postoperative pulmonary edema.
    • Dynamic measurements of volume status (pulse pressure variation, stroke volume variation) are useful for predicting fluid responsiveness and reducing inappropriate fluid administration

    Crystalloid Solutions and Clinical Use

    • Balanced salt solutions like Plasma-Lyte or Ringer’s lactate (LR) are commonly used for fluid resuscitation during surgery.
    • Their tonicity and electrolyte composition resemble extracellular fluid losses during surgery.
    • Hypotonic solutions (e.g., 0.45% NS) are often used for maintenance fluids, assuming free water losses predominate.
    • However, acute illness often increases ADH, predisposing patients to hyponatremia.
    • Current evidence suggests using isotonic or balanced salt solutions for maintenance fluids to minimize this risk.
    • 5% dextrose in maintenance fluids is inadequate for patients with prolonged malnutrition or significant malnourishment. Total parenteral nutrition is recommended in such cases.

    Normal Saline (NS)

    • Normal saline (NS) has a pH of approximately 5.5
    • When stored in polyvinyl chloride (PVC) packaged bags, the pH of NS can be as low as 4.6
    • NS contains 154 mEq/L of sodium and chloride

    Balanced Salt Solutions

    • Ringer’s lactate (LR) has a pH of 6.5
    • Plasma-Lyte has a pH of 7.4
    • LR contains lactate
    • Plasma-Lyte contains gluconate and acetate
    • Lactate, gluconate, and acetate are converted by the liver into bicarbonate

    Administration of Sodium Bicarbonate

    • Sodium bicarbonate may be added to 0.45% NS or 5% dextrose solution to create an alkalotic crystalloid solution
    • 1 ampule of 8.4% sodium bicarbonate contains 1 mEq/mL
    • Sodium bicarbonate increases a solution’s osmolarity by 2 mOsm/L for every 1 mL added

    Disadvantages of Normal Saline

    • NS can cause hyperchloremic metabolic acidosis
    • NS contributes to hyperkalemia in patients with end-stage renal disease (ESRD)

    Balanced Salt Solutions in Patients with ESRD

    • LR and Plasma-Lyte result in less hyperkalemia than NS
    • LR and Plasma-Lyte are recommended over NS in patients with ESRD due to the associated metabolic acidosis

    LR and Blood Products

    • LR contains calcium
    • LR should be avoided when transfusing blood products unless emergent

    Colloids vs. Crystalloids

    • Colloids have a long intravascular half-life (3 to 6 hours)
    • Crystalloids have an intravascular half-life of 20 to 40 minutes
    • Crystalloids are recommended over colloids for fluid resuscitation
    • Colloids can accumulate in the interstitial space and lead to edema

    Albumin Solutions

    • 5% albumin solution has a colloid osmotic pressure of about 20 mmHg
    • 25% albumin solution has a colloid osmotic pressure of about 5 times that of normal plasma

    Hypertonic Saline

    • Hypertonic saline (3%) has an osmolarity of 900 mOsm/L
    • Hypertonic saline is used for treating hyponatremia and elevated intracranial pressure (ICP)
    • Hypertonic saline helps decrease cerebral edema and reduce ICP

    Third-Space Losses

    • Third-space losses refer to fluid sequestration into a non-functional space
    • These losses occur in situations like major surgery, burns, and sepsis
    • Third-spacing necessitates further fluid infusions to maintain adequate intravascular volume

    Hyponatremia

    • Hyponatremia is classified based on the patient’s serum osmolality and volume status
    • The most common cause of hyponatremia is impaired renal excretion of water
    • Treatment depends on the severity and cause of hyponatremia
    • Correction of hyponatremia should occur slowly, with serial sodium concentrations measured
    • Rapid correction of hyponatremia can lead to osmotic demyelination syndrome
    • Osmotic demyelination syndrome typically develops within two to six days after rapid sodium correction

    Hypernatremia

    • Hypernatremia is less common than hyponatremia
    • Hypernatremia is always associated with hypertonicity
    • The level of total body sodium content dictates the treatment for hypernatremia

    Hypernatremia

    • Hypernatremia is often caused by decreased access to free water, particularly in elderly or debilitated patients with impaired thirst and decreased oral intake.
    • Other causes include central diabetes insipidus (lack of antidiuretic hormone) and nephrogenic diabetes insipidus (lack of response to antidiuretic hormone).
    • In hospitalized patients, hypernatremia is frequently iatrogenic, caused by excess sodium intake from intravenous fluids (e.g., normal saline) or medications (e.g., sodium bicarbonate, 3% sodium chloride).
    • Hypernatremia increases the minimal alveolar concentration for inhaled anesthetics.
    • Hypernatremia is commonly associated with fluid deficits, which must be corrected slowly to prevent cellular edema.
    • Elective surgery should be delayed if serum sodium levels exceed 150 mEq/L.

    Hypokalemia

    • A normal serum potassium level is approximately 3.5 to 5.0 mEq/L.
    • Hypokalemia represents significant total body potassium depletion, which can occur due to gastrointestinal or renal losses, transcellular shifts, or inadequate intake.
    • Gastrointestinal loss of potassium is often caused by diarrhea, but can also be triggered by laxative overuse and acute, colonic pseudoobstruction.
    • Renal potassium loss is associated with diuretics (especially loop diuretics) and certain types of renal tubular acidosis (types 1 and 2).
    • β-adrenergic agonists, insulin, and elevated serum pH can shift potassium intracellularly.
    • Hypokalemia can be seen in pregnant women receiving tocolytic therapy or patients on inotropic support due to the use of β-agonists.
    • Hypokalemia can occur in patients with inadequate potassium intake, but this often exacerbates hypokalemia from another etiology.
    • Hypokalemia can cause electrocardiogram abnormalities (ST segment and T wave depression, prolonged QT, and onset of U waves) and cardiac arrhythmias (premature ventricular contractions and atrial fibrillation).
    • It impairs cardiac contractility.
    • Hypokalemia can cause muscle weakness, including respiratory muscle weakness, and increase sensitivity to muscle relaxants.
    • Hypokalemia increases the risk of ileus and, if prolonged, can cause damage to the kidneys.

    Hypokalemia Treatment

    • Rapid correction of hypokalemia is not recommended as it can lead to cardiac arrest.
    • Patients without risk factors and not undergoing major procedures can tolerate hypokalemia to 3 mEq/L and possibly as low as 2.5 mEq/L.
    • Potassium repletion is often guided by the heuristic that every 10 mEq of potassium administered increases serum potassium by approximately 0.1 mEq/L.
    • Infusion limits for potassium are typically 20 mEq/h via a central line or 10 mEq/h via a peripheral line due to the risk of vein damage and discomfort.
    • Injectable potassium chloride should never be given undiluted or as a bolus, and no more than 20 mEq should be connected to intravenous lines.
    • Mild and asymptomatic hypokalemia can be treated with oral potassium replacement.

    Hyperkalemia

    • Hyperkalemia is defined as a serum potassium greater than 5.0 mEq/L, but symptoms usually don't develop until the level is 5.5 mEq/L or higher.
    • Symptoms of hyperkalemia include profound weakness and cardiac conduction abnormalities (enhanced automaticity and repolarization irregularities).
    • Peaked T waves are usually the earliest finding on electrocardiogram.
    • Increasing potassium levels are associated with progressive widening of the P wave, lengthening of the PR segment, QRS prolongation, conduction blocks, bradycardia, and ventricular arrhythmias.
    • Development of a sine wave appearance on telemetry or electrocardiogram is usually a precursor to cardiac arrest.

    Hyperkalemia Causes

    • Hyperkalemia can be acute or chronic.
    • Causes include increased intake, decreased excretion, and transcellular shifts due to low serum pH.
    • Increased intake is often iatrogenic, caused by potassium supplementation or potassium-containing medications.
    • Medications that can cause hyperkalemia include angiotensin antagonists and receptor blockers, potassium-sparing diuretics (e.g., spironolactone and triamterene), and succinylcholine.
    • Increased potassium release from cells can occur with severe trauma, rhabdomyolysis, hemolysis, tumor lysis, and massive transfusion.
    • Decreased excretion of potassium is most common due to renal dysfunction, which can be acute or chronic.

    Hyperkalemia after Succinylcholine

    • Serum potassium can increase by approximately 0.5 mEq/L after routine administration of succinylcholine, therefore it should be avoided in patients who are already hyperkalemic.
    • Other patients who may be susceptible to an exaggerated potassium response include those with spinal cord or denervation injuries, stroke, head injuries, significant burns, rhabdomyolysis, intraabdominal infections, and immobility.
    • Conservatively, succinylcholine should be avoided in patients with burns, stroke, or spinal cord injury after 24 hours.

    Hyperkalemia Treatment

    • Hyperkalemia greater than 6 mEq/L should be corrected before elective procedures.
    • Dialysis is usually the preferred treatment.
    • Intermittent hemodialysis offers faster clearance and may be preferred over continuous renal replacement therapies for patients with significant or symptomatic hyperkalemia.
    • Cardiotoxicity (changes on electrocardiogram or telemetry) is treated with intravenous calcium chloride or calcium gluconate.
    • Rapid intracellular potassium shift can be achieved with β-adrenergic stimulation (e.g., inhaled albuterol) and intravenous insulin (typically given with intravenous dextrose supplementation).
    • In patients with acidemia, hyperventilation and sodium bicarbonate can also help shift potassium intracellularly.
    • Excretion of potassium can be accomplished using diuretics, sodium polystyrene sulfonate (Kayexalate), and dialysis.
    • Intravenous fluids (normal saline) can also be helpful in hypovolemic patients.

    Hypocalcemia

    • Major causes of hypocalcemia include hypoparathyroidism, hyperphosphatemia, vitamin D deficiency, malabsorption, rapid blood transfusion, pancreatitis, rhabdomyolysis, and fat embolism.
    • Hypocalcemia is a concern after thyroidectomy if no parathyroid tissue is left, potentially leading to laryngeal spasms and stridor.

    Hypocalcemia Manifestations

    • Hypocalcemia impairs cardiac contractility, resulting in hypotension.
    • Serial ionized calcium levels should be checked in patients receiving multiple blood transfusions to ensure hypocalcemia is not contributing to shock.
    • Hypocalcemia can cause QT prolongation, but conduction abnormalities are less common than with other electrolyte abnormalities.
    • Other possible symptoms include tetany, perioral paresthesias, seizures, anxiety, and confusion.
    • Trousseau's sign and Chvostek's sign may be found on examination.

    Ionized Calcium

    • Total serum calcium levels may not accurately reflect the ionized (free) calcium level, which is clinically more important.
    • Each 1 g/dL reduction in serum albumin concentration lowers total calcium concentration by approximately 0.8 mg/dL, but does not affect ionized calcium concentration.
    • The affinity of calcium for albumin is higher in the setting of alkalosis, so ionized calcium may be decreased in patients with an elevated serum pH.

    Hypocalcemia Treatment

    • Acute hypocalcemia is treated with intravenous calcium chloride or calcium gluconate, but always address the underlying cause.
    • Calcium chloride provides more active calcium than gluconate, but calcium gluconate may be preferable for patients without central access due to lower irritation and risk of tissue necrosis if extravasation occurs.

    Magnesium

    • A typical serum magnesium level is 1.3 to 2.2 mEq/L.
    • Hypomagnesemia causes QT prolongation and can lead to torsades de pointes and other arrhythmias.
    • Other symptoms of hypomagnesemia include muscle weakness, tremors, twitches, numbness, and paresthesias.
    • Severe hypomagnesemia can cause confusion, drowsiness, and seizures.
    • Hypermagnesemia is uncommon and usually caused by renal dysfunction or excessive intake.
    • Symptoms of magnesium toxicity typically occur at levels of 4 to 6 mEq/L and include nausea, headache, drowsiness, and decreased deep tendon reflexes.
    • As magnesium levels increase, patients develop muscle weakness, respiratory insufficiency and failure, absent deep tendon reflexes, hypotension, bradycardia, and possible cardiac arrest.

    Hypomagnesemia and Anesthesia

    • Hypomagnesemia is increasingly recognized in patients with gastrointestinal losses, malnutrition, alcohol addiction, or critical illness.
    • Hypomagnesemia is often associated with hypokalemia and hypophosphatemia.
    • Hypokalemia is often difficult to correct unless hypomagnesemia is also treated.
    • Patients with hypomagnesemia have increased susceptibility to muscle relaxants and may experience weakness after surgery, potentially leading to respiratory insufficiency.
    • Hypomagnesemia can also impair cardiac contractility and cause dysrhythmias (e.g., torsades de pointes).
    • Patients undergoing massive resuscitation are at risk for hypomagnesemia and should be given magnesium chloride (1-2 g) if dysrhythmias or refractory hypotension develop.

    Hyperchloremia

    • Hyperchloremia has been increasingly recognized after administration of 0.9% normal saline.
    • Patients undergoing prolonged surgeries or those with septic shock or significant trauma are most likely to be impacted due to their need for large-volume fluid resuscitation.
    • Hyperchloremia causes a nonanion gap metabolic acidosis.

    Autonomic Nervous System

    • The autonomic nervous system controls involuntary bodily functions, maintaining internal homeostasis and responding to stress.
    • Consists of three components: sympathetic, parasympathetic, and enteric nervous systems.
    • Sympathetic nervous system (SNS) produces widespread effects, while the parasympathetic nervous system (PNS) tends to have more localized effects.
    • SNS and PNS generally have opposing effects on most organs.
    • The PNS predominates at rest (rest-and-digest), while the SNS predominates in stressful situations (fight-or-flight).

    Sympathetic Nervous System Anatomy

    • Preganglionic neurons originate in the spinal cord (T1-L2).
    • Synapse with three types of ganglia: paravertebral, prevertebral, and adrenal medulla.
    • Paravertebral ganglia form a chain along the vertebral column, from the skull to the coccyx.
    • Prevertebral ganglia are located anterior to the vertebral column.
    • Adrenal medulla directly secretes catecholamines into the bloodstream.

    Sympathetic Innervation

    • Preganglionic sympathetic neurons can ascend or descend the sympathetic chain, synapsing with multiple ganglia.
    • Release acetylcholine at their synapse with postganglionic neurons.
    • Postganglionic neurons release norepinephrine (NE), except for sweat glands which release acetylcholine.

    Interventional Pain Management

    • Stellate ganglia: paired paravertebral ganglia innervating the head, neck, and upper extremities.
    • A common target for nerve blocks to treat complex regional pain syndrome of the upper extremity.
    • Celiac Plexus: a collection of prevertebral ganglia innervating the stomach, liver, spleen, pancreas, kidneys, and GI tract.
    • A common target for nerve blocks to treat complex abdominal pain disorders, such as pancreatic cancer.

    Parasympathetic Nervous System Anatomy

    • Preganglionic neurons originate from cranial nerves III, VII, IX, X and sacral segments S2 to S4.
    • Vagus nerve carries approximately 75% of PNS traffic.
    • Synapse with postganglionic neurons close to the target organ, facilitating fine, discrete physiological effects.
    • Both preganglionic and postganglionic parasympathetic neurons release acetylcholine.

    Adrenergic Receptors

    • Alpha-1 (α1), alpha-2 (α2), beta-1 (β1), and beta-2 (β2).
    • α1, β1, and β2 receptors are postsynaptic and stimulated by NE.
    • α2 receptors are presynaptic and stimulated by NE, inhibiting presynaptic release of NE.

    Catecholamines

    • Monoamines that stimulate adrenergic nerve terminals.
    • Naturally occurring: NE, epinephrine, and dopamine.
    • Synthetic: dobutamine and isoproterenol.

    Catecholamine Synthesis

    • Tyrosine is converted to dopamine through two enzymatic reactions: hydroxylation by tyrosine hydroxylase, and decarboxylation by aromatic l-amino acid decarboxylase.
    • Dopamine is transported into storage vesicles and hydroxylated by dopamine β-hydroxylase to NE.
    • Epinephrine is synthesized in the adrenal medulla from NE through methylation by phenylethanolamine N-methyltransferase.

    Catecholamine Metabolism

    • NE is primarily removed from the synaptic junction by reuptake, but a small amount enters circulation and undergoes metabolism.
    • Metabolized in the blood, liver, and kidney by monoamine oxidase and catecholamine O–methyltransferase.
    • Metabolites of epinephrine and NE are metanephrine and normetanephrine, respectively.

    Importance of Catecholamine Metabolites

    • Catecholamines have a short half-life (t1/2 ≈ 2 minutes).
    • Their metabolites have a longer half-life (t1/2 ≈ 1–2 hours).
    • Metanephrine and normetanephrine are used to diagnose pheochromocytoma.

    Acetylcholine Metabolism

    • Rapidly metabolized to choline and acetate by acetylcholinesterase (AChE).

    Cholinergic Crisis

    • Accumulation of acetylcholine due to AChE inhibition.
    • Side effects: bradycardia, salivation, lacrimation, urination, defecation, emesis, even more severe effects like bronchoconstriction, blindness, and muscular paralysis.
    • Treatment involves atropine and intubation for respiratory support.

    Beta-Adrenergic Antagonists (Beta Blockers)

    • Antagonize β1 and β2 receptors.
    • Commonly used for hypertension, angina, dysrhythmias.
    • Used perioperatively to reduce death after myocardial infarction.

    Mechanism of Action and Side Effects of Beta Blockers

    • β1 and β2 antagonism decreases adenylate cyclase activation, reducing cAMP production.
    • β1-Blockade: negative chronotropic and inotropic effects, decreasing heart rate, contractility, cardiac output, and myocardial oxygen requirement.
    • β1-Blockers also reduce renin secretion, lowering fluid retention and angiotensin II.
    • Can cause hyperkalemia.
    • May decrease signs of hypoglycemia.
    • Abrupt withdrawal can lead to hypertension, tachycardia, and myocardial ischemia.

    Beta-2 Antagonism

    • β2 receptors located on vascular and bronchial smooth muscle.
    • β2-Blockade causes peripheral vasoconstriction, bronchoconstriction, inhibition of insulin release and glycogenolysis.
    • Selective β1 blockers should be used in patients with peripheral vascular disease, COPD, or reactive airway disease.

    Beta Blockade and the Surgical Stress Response

    • β antagonism can attenuate the adrenergic response to surgical stress, but its effectiveness in protecting patients from harm is unclear.

    Complications of Beta Blockade Treatment

    • Bradycardia and heart block: typically respond to atropine or glycopyrrolate.
    • Refractory cases: require β1-agonism with epinephrine, dobutamine, or isoproterenol.
    • Other options: glucagon, calcium, insulin and glucose, and lipid emulsion therapy.

    Alpha-2 Agonists

    • Inhibit adenylate cyclase, decreasing cAMP production.
    • Reduce sympathetic outflow from presynaptic nerve terminals in the CNS.
    • Dexmedetomidine: commonly used in the perioperative setting, producing sedation, analgesia, and reducing anesthetic requirement, heart rate, and blood pressure.
    • Side effects include bradycardia.
    • Clonidine: used as an antihypertensive, but can lead to rebound hypertension if stopped abruptly.

    Muscarinic Antagonists for Neuromuscular Blockade Reversal

    • Nondepolarizing muscle relaxants can be reversed with AChE inhibitors, but these also increase ACh at muscarinic receptors, causing side effects.
    • Muscarinic antagonists (e.g., glycopyrrolate) minimize these side effects by antagonizing ACh at muscarinic receptors.

    Glycopyrrolate

    • Most frequently administered muscarinic antagonist.
    • Quaternary amine, does not readily cross the blood-brain barrier, minimizing CNS side effects.

    Autonomic Dysfunction

    • Patients with ANS dysfunction or dysautonomia are at risk of severe hypotension and aspiration from gastroparesis.
    • Risk factors: diabetes mellitus and chronic alcohol abuse.

    Spinal Cord Injury and the Autonomic Nervous System

    • Causes various ANS issues depending on the site, extent, and timing of the lesion.
    • High spinal cord injury (T6 or above) can lead to exaggerated SNS responses due to loss of supraspinal feedback.
    • Spinal shock: initial stage with vasodilation and compensatory tachycardia.
    • Chronic injury: may result in hypotension and bradycardia.
    • Upregulation of adrenergic receptors can make patients sensitive to vasopressors.
    • Autonomic dysreflexia: pressure stimuli below the level of the lesion can cause hypertension and bradycardia.

    Pheochromocytoma

    • Catecholamine-secreting tumor causing paroxysmal hypertension, tachycardia, headache, and diaphoresis.
    • Diagnosed by detecting elevated levels of metanephrine and normetanephrine.

    Vessel Compliance

    • Ability of a vessel to distend for a given pressure.
    • Veins have higher compliance than arteries due to lack of muscular stiffness.
    • Artery stiffness increases with age, reducing compliance.
    • Stiff arteries contribute to hypertension and reduce the body's ability to respond to hemorrhage.
    • Veins store two-thirds of the blood volume and can be recruited in situations like hypovolemia.

    Hemorrhage and the Physiological Response

    • Increased sympathetic tone stimulates α1 adrenergic receptors, causing venoconstriction and decreasing venous compliance to maintain preload.
    • Age affects the response due to decreased arterial compliance and overall reduced physiological reserve.

    Hemorrhage and Sympathetic Response

    • Sympathetic tone increases in hemorrhage to maintain blood pressure and cardiac output.
    • This releases norepinephrine and epinephrine, which stimulate α1 adrenergic receptors on arteries and veins.
    • Arterial stimulation increases systemic vascular resistance.
    • Venous stimulation decreases venous compliance, increasing venous return and preload.
    • Catecholamines also increase heart rate and contractility to maintain cardiac output.
    • Younger patients have greater physiological reserve and tolerate larger blood loss before vital sign changes.
    • Older patients have decreased reserve due to atherosclerosis, reduced cardiac function, and medications like β blockers.

    Heart Structure and Function

    • The heart is a muscular organ responsible for pumping blood to the body.
    • It has four chambers: two atria and two ventricles.
    • The heart is divided into right and left sides.
    • Each chamber is separated by a one-way valve.

    Lung Volumes and Capacities

    • Tidal volume (TV): Volume of gas inhaled and exhaled during normal breathing.
    • Expiratory reserve volume (ERV): Volume of gas exhaled after a normal breath.
    • Residual volume (RV): Volume of gas remaining after maximal exhalation.
    • Functional residual capacity (FRC): ERV + RV.
    • Inspiratory reserve volume (IRV): Volume of gas inhaled above a tidal breath.
    • Inspiratory capacity (IC): IRV + TV.
    • Vital capacity (VC): IRV + TV + ERV.
    • Total lung capacity (TLC): IRV + TV + ERV + RV.

    Body Water Compartments

    • Total body water is approximately 60% of body weight.
    • Two-thirds (intracellular fluid) and one-third (extracellular fluid) comprise the body water compartments.
    • Extracellular fluid is further divided into interstitial fluid (three-quarters) and plasma (one-quarter).
    • This can be remembered as the "20-40-60" rule: 20% extracellular, 40% intracellular, 60% total body water.

    Fluid Distribution Between Plasma and Endothelial Glycocalyx

    • Sterling's principle describes filtration between the intravascular and interstitial spaces.
    • The endothelial glycocalyx is a layer in the capillaries that contributes to fluid transfer.
    • Revised Starling's principle accounts for the glycocalyx and proposes filtration occurs throughout the capillary bed.
    • Reabsorption from the interstitial space may not occur.
    • Net filtration is governed by the glycocalyx, endothelial basement membrane, and extracellular matrix.

    Serum Osmolarity

    • Normal serum osmolarity ranges between 285 and 305 mOsm/L.
    • A quick estimate is to double the sodium concentration.
    • A more accurate estimate can be obtained using a calculation with sodium, glucose, and BUN values.

    Body Water and Tonicity Regulation

    • The kidney's response to antidiuretic hormone (ADH) regulates body water and tonicity.
    • ADH increases water permeability in renal tubules, concentrating urine and conserving water.
    • ADH release is stimulated by hyperosmolarity, hypotension, hypovolemia, and stress.
    • Hypovolemia and hypotension take precedence over osmolarity.

    ADH Synthesis and Release

    • ADH is synthesized in the hypothalamus and stored in the posterior pituitary.
    • It is released in response to stimuli from osmoreceptors and baroreceptors.

    Factors Affecting ADH Release

    • Stimuli for ADH release: hyperosmolarity, hypovolemia, upright position, β-adrenergic stimulation, pain, stress, and cholinergic stimulation.
    • Inhibitors of ADH release: hypoosmolarity, hypervolemia, supine position, α-adrenergic stimulation, excess water intake, hypothermia, medications like ethanol and atropine.

    Diabetes Insipidus (DI)

    • DI is characterized by excessive urination of dilute urine due to ADH deficiency or resistance.
    • It can be classified as neurogenic (impaired ADH release) or nephrogenic (renal resistance to ADH).
    • Diagnosis includes fluid restriction testing and ADH measurements.
    • Treating neurogenic DI involves ADH replacement therapy.
    • Neprogenic DI is usually managed with fluid replacement and medications.

    Causes of DI

    • Neurogenic DI: familial, acquired, idiopathic, craniofacial fractures, pituitary tumors, granulomas, infections, brain injury, and pituitary surgery.
    • Nephrogenic DI: familial, acquired, pyelonephritis, renal obstruction, sickle cell disease, amyloidosis, hypokalemia, hypercalcemia, sarcoidosis, and medications like lithium.

    Management of Central DI

    • ADH replacement therapy with desmopressin (DDAVP) or vasopressin.
    • Hypotonic maintenance fluids are used.
    • Avoid isotonic fluids (NS) as they can worsen hypernatremia.
    • Incomplete DI might be managed with thiazide diuretics or chlorpropamide.
    • Monitoring of plasma and urine osmolarity, as well as urine output, is important.

    Syndrome of Inappropriate ADH (SIADH)

    • SIADH is characterized by serum hypotonicity caused by nonosmotic ADH release.
    • Diagnosis requires: euvolemia or hypervolemia, concentrated urine, normal renal, cardiac, hepatic, adrenal, and thyroid function.

    Managing SIADH

    • Primary therapy is water restriction.
    • Severe symptomatic hyponatremia requires intensive care and possibly hypertonic saline.
    • Avoid normal saline as it worsens hyponatremia.
    • Chronic SIADH might require demeclocycline or vaptans.

    Disorders Associated with SIADH

    • Central nervous system conditions (head injury, tumors, meningitis, subarachnoid hemorrhage).
    • Pulmonary conditions (tuberculosis, pneumonia, asthma, bronchiectasis).
    • Malignancies (ADH-like compound secretion).
    • Adrenal insufficiency and hypothyroidism.

    Stress-Induced Hyponatremia

    • Stressful situations (surgery, critical illness) increase sympathetic tone, leading to ADH release and renin-angiotensin-aldosterone system activation.
    • This causes free water reabsorption, decreasing urine output despite normal volume status.
    • This can result in mild dilutional hyponatremia.
    • Urine output is a poor indicator of volume status in these situations.

    Aldosterone

    • Aldosterone controls sodium excretion.
    • Renin release from the kidneys is stimulated by decreased blood pressure, hypovolemia, and hyponatremia.
    • Renin converts angiotensinogen to angiotensin I, which is converted to angiotensin II by angiotensin-converting enzyme.
    • Angiotensin II stimulates aldosterone release from the adrenal cortex.
    • Other effects of angiotensin II include vasoconstriction and ADH release.
    • Aldosterone promotes sodium reabsorption and potassium excretion in the kidneys.

    Perioperative Fluid Status Derangements

    • Preoperative hypovolemia: bowel prep, blood loss, sepsis, pancreatitis, or small bowel obstruction.
    • Intraoperative factors: anesthetic medications and procedures (vasodilation), procedure-related blood loss, evaporative losses, and third-spacing.

    Consequences of Hypovolemia (or Hypervolemia)

    • Hypovolemia can lead to decreased cardiac output, tissue perfusion, and shock.
    • Hypervolemia can lead to pulmonary edema, bowel edema, wound edema, and coagulation factor dilution.
    • Optimal volume resuscitation is crucial.

    Contraction Alkalosis

    • Contraction alkalosis (chloride depletion alkalosis) often occurs in patients with hypovolemia and hypochloremia.
    • Caused by conditions such as diuretic use, upper gastrointestinal losses, and volume depletion.
    • Treatment involves chloride and volume resuscitation.

    Fluid Administration during Surgery

    • Avoid overresuscitation based on imprecise fluid loss estimates.
    • Restrictive fluid maintenance (3-5 mL/kg/h) is associated with better outcomes compared to liberal fluid resuscitation (10-12 mL/kg/h) in abdominal surgery.
    • Fluid restriction is particularly important in thoracic surgery.
    • Dynamic measurements (pulse pressure variation, stroke volume variation) help predict fluid responsiveness and minimize unnecessary fluid administration.

    Crystalloid Solutions

    • Balanced salt solutions (Plasma-Lyte, Ringer's lactate) are preferred for fluid resuscitation.
    • Hypotonic solutions (0.45% NS) are often used for maintenance fluids.
    • However, isotonic or balanced salt solutions are recommended in acutely ill patients to minimize hyponatremia risk.
    • Maintenance fluids often include 5% dextrose to prevent hypoglycemia and tissue catabolism.

    Other Key Points

    • Accurate estimations of body water compartments can be difficult in obese patients.
    • Fasting for 10+ hours before surgery does not contribute to significant hypovolemia.
    • Lowering anesthetic depth or administering vasopressors can help minimize fluid needs before volume resuscitation.
    • Urine output is not a reliable indicator of intraoperative volume status.
    • Total parenteral nutrition is needed for prolonged malnutrition.
    • Optimizing, not maximizing, intravascular volume is the goal during surgery.

    The Composition of Isotonic Crystalloid Solutions

    • Normal Saline (NS): Osmolarity of 308, pH of 5.5, Contains 154 mEq/L of Sodium and Chloride
    • Lactated Ringer's (LR): Osmolarity of 273, pH of 6.5, Contains 130 mEq/L of Sodium, 109 mEq/L of Chloride, 4 mEq/L of Potassium, 3 mEq/L of Calcium, 28 mEq/L of Lactate
    • Plasma-Lyte: Osmolarity of 294, pH of 7.4, Contains 140 mEq/L of Sodium, 98 mEq/L of Chloride, 5 mEq/L of Potassium, 3 mEq/L of Magnesium, 27 mEq/L of Acetate, 23 mEq/L of Gluconate

    The pH of Normal Saline

    • Normal saline has a pH of 5.5 due to dissolved carbon dioxide from atmospheric air reacting with water to form carbonic acid
    • The use of polyvinyl chloride (PVC) packaging further lowers the pH because PVC produces hydrochloric acid when moist

    Balanced Salt Solutions

    • Balanced salt solutions, like LR and Plasma-Lyte, have pH values closer to plasma pH (7.4)
    • LR contains lactate, which the liver converts to bicarbonate
    • Plasma-Lyte contains gluconate and acetate, which are also converted to bicarbonate by the liver

    Use of Bicarbonate in Crystalline Solutions

    • Bicarbonate is not used in manufactured crystalloid solutions because it reacts with water to form carbon dioxide, which diffuses out of the solution and packaging
    • Bicarbonate can also precipitate with calcium and magnesium, which is problematic

    Creating a Crystalloid Solution for Metabolic Acidosis

    • Sodium bicarbonate can be added to 0.45% NS or 5% dextrose solution to create an alkaline crystalloid solution for immediate use
    • For example, one 50 mL ampule of 8.4% sodium bicarbonate can be mixed with 1 L of 5% dextrose or 0.45% half-NS to produce a solution with similar or higher pH than balanced salt solutions
    • Adding 1.5 ampules of sodium bicarbonate to 1 L of 0.45% saline will yield an approximate osmolarity of 304 mOsm/L
    • Adding 3 ampules of sodium bicarbonate to 1 L of 5% dextrose solution will yield an isotonic solution with an osmolarity of 300 mOsm/L

    Disadvantages of Normal Saline

    • NS contains high levels of sodium and chloride, exceeding those found in normal plasma
    • NS has a low pH (4.6 to 5.5), leading to hyperchloremic metabolic acidosis when administered in large volumes

    Advantages of Balanced Salt Solutions

    • Balanced salt solutions contain additional electrolytes like magnesium, potassium, and calcium that are closer to the composition of extracellular fluid
    • They can be used for patients with end-stage renal disease (ESRD) with less risk of hyperkalemia compared to NS

    Administration of Lactated Ringer's (LR) with Blood Products

    • LR contains calcium, which could theoretically cause clotting in blood products since they are treated with chelating agents like citrate to prevent clotting during storage
    • LR should ideally be avoided when transfusing blood products, unless it's an emergency situation

    Colloids Vs. Crystalloids for Resuscitation

    • There is ongoing debate whether colloids are superior to crystalloids for resuscitation
    • While advocates claim that colloids have a longer intravascular half-life, studies don't demonstrate improved outcomes compared to crystalloids
    • Colloids can accumulate in the interstitial space with increased capillary permeability, leading to edema

    Intravascular Half-Lives

    • Crystalloids have a short intravascular half-life of 20-40 minutes
    • Albumin has a longer half-life of 3-6 hours

    Volume Replacement with Crystalloids Vs. Colloids

    • 1 L of isotonic crystalloid will increase the intravascular space by 250 mL, similar to one standard unit of 5% albumin solution
    • Crystalloids primarily increase the extracellular space, while colloids primarily increase the intravascular space

    Albumin Solutions

    • Two main albumin preparations: 5% and 25% albumin solution
    • Both preparations are highly unlikely to be contaminated with pathogens, with only a theoretical risk of prion disease
    • 5% albumin has a colloid osmotic pressure similar to plasma (20 mmHg)
    • 25% albumin has a higher colloid osmotic pressure (5 times normal plasma) and a smaller standard volume (50 mL vs 250 mL)

    Albumin for Volume Replacement

    • In the perioperative environment, albumin is rarely indicated for volume replacement or normalization of serum albumin
    • Albumin may be considered in hypervolemic patients who are volume responsive, known as the "hypervolemic intravascular depleted state"

    Uses of Hypertonic Saline

    • Hypertonic saline (3%) is used for patients in hypovolemic shock, to reduce the need for crystalloids during large operations, and to treat hyponatremia and elevated intracranial pressure (ICP)
    • It helps decrease cerebral edema by reducing the amount of water that crosses the blood-brain barrier
    • Hypertonic saline is given in 100-250 mL boluses over 10-30 minutes, titrated to mental status, ICP, and sodium levels
    • Higher concentrations (23%) may be used when brain herniation is imminent

    Third-Space Losses

    • Third-space losses refer to fluid sequestration into an inactive "third space" in conditions like major surgery, hemorrhagic shock, burns, and sepsis
    • This fluid does not participate in microcirculatory exchanges and does not contribute to cardiac output or tissue perfusion
    • These losses necessitate additional fluid infusions to maintain adequate intravascular volume
    • These losses typically resolve once the underlying primary problem has been treated

    Key Points in Volume Regulation and Fluid Replacement

    • Estimating volume status requires comprehensive clinical information as multiple variables can be misleading
    • Replace intraoperative fluid losses with isotonic fluids
    • Contraction alkalosis, or chloride deficient alkalosis, requires replenishing both volume and chloride levels, typically with NS
    • Large quantities of NS can cause hyperchloremic metabolic acidosis and should not be the primary fluid for volume resuscitation.
    • Balanced salt solutions, such as LR and Plasma-Lyte, are ideal for volume resuscitation and can be used for maintenance fluids and patients with ESRD
    • Albumin has not consistently shown to improve outcomes over crystalloids and may increase mortality in patients with traumatic brain injuries

    Hyponatremia Classification

    • Hyponatremia is classified based on serum osmolality and volume status
    • It can occur with low serum osmolality (<295 mOsm/kg) due to increased total body water
    • This is typically caused by impaired renal water excretion, but can be due to excessive water intake
    • Causes of hyponatremia include diuretics, renal tubular acidosis, hypoaldosteronism, salt-wasting nephropathies, vomiting, diarrhea, syndrome of inappropriate antidiuretic hormone (SIADH), hypothyroidism, and cortisol deficiency

    Causes of Acute Hyponatremia in the Operating Room

    • Administration of hypotonic fluids (e.g., irrigation solutions like glycine and sorbitol)
    • Use of mannitol, especially in patients with renal dysfunction

    Symptoms of Acute Hyponatremia

    • Nausea, vomiting, visual disturbances, muscle cramps, weakness, bradycardia
    • Elevated intracranial pressure (ICP) resulting in mental status changes (apprehension, agitation, confusion, obtundation)
    • Seizures with severe hyponatremia (<120 mEq/L)

    Hyponatremia During Planned Elective Procedures

    • Mild hyponatremia (≥130 mEq/L) without symptoms should not result in cancellation of a planned procedure, as long as worsening is not expected

    Treatment of Acute Hyponatremia

    • Fluid restriction is usually sufficient for mild cases
    • Loop diuretics may be indicated
    • Correction should be slow with serial sodium measurements
    • For asymptomatic patients with sodium <130 mEq/L, sodium should be corrected at a rate of ≤0.5 mEq/L/h
    • Hypertonic saline is reserved for refractory hyponatremia or severe neurological symptoms
    • An initial bolus of 100 mL of 3% saline followed by two additional boluses over 30 minutes may be given.
    • Goal is to increase sodium 4-6 mEq/L over a few hours to decrease ICP and resolve neurological symptoms

    Safe Correction Rate for Hyponatremia

    • Increase sodium should not exceed 10-12 mEq/L/day to prevent osmotic demyelination syndrome
    • A slower correction rate (4-6 mEq/L/day) may be safer, especially in asymptomatic patients
    • Rapid correction is safer with neurological symptoms as long as it doesn't exceed a few hours
    • Osmotic demyelination syndrome is rare in patients with initial sodium level higher than 120 mEq/L

    Symptoms of Osmotic Demyelination Syndrome

    • Neuromuscular symptoms develop 2-6 days after rapid changes in sodium: confusion, movement disorders, obtundation, seizures, weakness, myoclonic jerks
    • Often irreversible

    Osmotic Demyelination Syndrome in Specific Patient Groups

    • Females of reproductive age, especially during menstruation, have higher risk of neurological sequelae
    • Patients with prolonged hyponatremia (over 2 days) are more vulnerable

    Etiologies of Hypernatremia

    • Less common than hyponatremia
    • Always associated with hypertonicity
    • Can occur with low, normal, or high total body sodium content
    • Causes include dehydration, excessive sodium intake, renal failure, and diabetes insipidus.

    Hypernatremia

    • Hypernatremia is often a result of decreased access to free water, especially in elderly or debilitated patients with impaired thirst and decreased oral intake.
    • Other causes include central diabetes insipidus (lack of antidiuretic hormone) and nephrogenic diabetes insipidus (lack of response to antidiuretic hormone).
    • In hospitalized patients, hypernatremia can be iatrogenic due to excess sodium intake from intravenous fluids (normal saline) or medications like sodium bicarbonate or 3% sodium chloride.
    • Hypernatremia increases minimal alveolar concentration for inhaled anesthetics.
    • Hypernatremia often accompanies fluid deficits, which must be corrected slowly to prevent cellular edema.
    • Elective surgery should generally be delayed if serum sodium levels exceed 150 mEq/L.

    Potassium

    • Normal serum potassium concentration is in the approximate range of 3.5 to 5.0 mEq/L.
    • Hypokalemia can occur due to gastrointestinal or renal losses, transcellular shifts, or inadequate intake.
    • Gastrointestinal loss of potassium is often caused by diarrhea, laxative overuse, or acute colonic pseudoobstruction.
    • Renal losses can occur due to diuretics (especially loop diuretics) and some forms of renal tubular acidosis.
    • Insulin, β-adrenergic agonists, and high serum pH can shift potassium intracellularly.
    • Hypokalemia can cause electrocardiogram abnormalities, cardiac arrhythmias, and impaired cardiac contractility.
    • Hypokalemia also causes muscle weakness, increases sensitivity to muscle relaxants, and increases the risk of ileus.
    • Rapid potassium correction can be dangerous and lead to cardiac arrest.
    • Hypokalemic patients without risk factors can tolerate mild hypokalemia down to 3 mEq/L, and possibly as low as 2.5 mEq/L.

    Hyperkalemia

    • Hyperkalemia is defined as a serum concentration greater than 5.0 mEq/L, but symptoms typically don't develop until the level is 5.5 mEq/L or higher.
    • Hyperkalemia can produce profound weakness and cardiac conduction abnormalities, including enhanced automaticity and repolarization irregularities.
    • The earliest EKG finding is usually peaked T waves.
    • As potassium levels increase, P wave widening, PR segment lengthening, QRS prolongation, conduction blocks, bradycardia, and ventricular arrhythmias can occur.
    • Hyperkalemia can be acute or chronic and has several causes: increased intake, decreased excretion, and transcellular shifts due to low serum pH.
    • Iatrogenic hyperkalemia can occur due to potassium supplementation or potassium-containing medications.
    • Medications contributing to hyperkalemia: angiotensin antagonists, receptor blockers, potassium-sparing diuretics, and succinylcholine.
    • Hyperkalemia can also occur after increased potassium release from cells: severe trauma, rhabdomyolysis, hemolysis, tumor lysis, and massive transfusion.
    • Decreased potassium excretion is most common due to acute or chronic renal dysfunction.

    Succinylcholine and Hyperkalemia

    • Routine administration of succinylcholine can increase serum potassium by approximately 0.5 mEq/L.
    • Avoid succinylcholine in hyperkalemic patients and in patient populations susceptible to an exaggerated potassium response: spinal cord or denervation injuries, stroke, head injuries, burns, rhabdomyolysis, intraabdominal infections, and immobility.

    Hypocalcemia

    • Major causes of hypocalcemia include: hypoparathyroidism, hyperphosphatemia, vitamin D deficiency, malabsorption, rapid blood transfusion, pancreatitis, rhabdomyolysis, and fat embolism.
    • Hypocalcemia can cause laryngeal spasms and stridor after thyroidectomy if no parathyroid tissue is left.
    • Hypocalcemia impairs cardiac contractility, resulting in hypotension.
    • Hypocalcemia can cause QT prolongation and tetany (muscle spasms).
    • Other symptoms include: perioral paresthesias, seizures, anxiety, and confusion.
    • Trousseau’s sign (carpopedal spasm with cuff inflation) and Chvostek’s sign (facial muscle contraction with facial nerve tapping) are possible on examination.

    Hypocalcemia Treatment

    • Treatment of acute hypocalcemia involves intravenous calcium chloride or calcium gluconate.
    • The primary disturbance should also be addressed.
    • Calcium chloride provides more active calcium than calcium gluconate.
    • Calcium gluconate may be preferable in patients without central access due to less irritation and lower risk of tissue necrosis with extravasation.

    Magnesium

    • Normal serum magnesium level is 1.3 to 2.2 mEq/L.
    • Hypomagnesemia causes QT prolongation and can lead to torsades de pointes and other arrhythmias.
    • Other symptoms include: muscle weakness, tremors, twitches, numbness, paresthesias, confusion, drowsiness, and seizures.
    • Hypermagnesemia is typically caused by renal dysfunction or excessive intake (often iatrogenic).
    • Symptoms of magnesium toxicity occur at levels of 4 to 6 mEq/L and include: nausea, headache, drowsiness, decreased deep tendon reflexes, muscle weakness, respiratory insufficiency, absent deep tendon reflexes, hypotension, bradycardia, and possible cardiac arrest.

    Hypomagnesemia and Anesthesia

    • Hypomagnesemia is increasingly recognized in patients with gastrointestinal losses, malnutrition, alcoholism, and critical illness.
    • Hypomagnesemia commonly coexists with hypokalemia and hypophosphatemia.
    • Magnesium deficiency can exacerbate potassium excretion, making hypokalemia difficult to correct.
    • Hypomagnesemic patients are more susceptible to muscle relaxants, may have impaired cardiac contractility, and are at increased risk for dysrhythmias.

    Chloride

    • Hyperchloremia is associated with the use of 0.9% normal saline (contains 154 mEq/L of chloride).
    • Patients undergoing prolonged surgeries, septic shock, or significant trauma are most likely to be affected due to large-volume fluid resuscitation.
    • Hyperchloremia causes a nonanion gap metabolic acidosis.

    Key Points: Electrolytes

    • Electrolyte disturbances can be difficult to correct without treating the underlying cause.
    • Emergent treatment of hyponatremic patients with hypertonic saline should be reserved for those with severe, neurological symptoms.
    • Hypernatremia is often associated with fluid deficits, which must be addressed carefully to prevent cellular edema.
    • Cardiotoxicity due to hyperkalemia should be immediately treated with intravenous calcium chloride or calcium gluconate.
    • Patients receiving high volumes of fluid, especially normal saline, often develop hyperchloremia and a nonanion gap metabolic acidosis.

    Autonomic Nervous System

    • The autonomic nervous system (ANS) controls involuntary bodily functions like maintaining homeostasis and responding to stress.
    • The ANS is composed of the sympathetic nervous system (SNS), parasympathetic nervous system (PNS), and enteric nervous system (ENS).
    • The SNS generally produces widespread effects while the PNS produces more localized, discrete effects.
    • The SNS is responsible for the "fight-or-flight" response, while the PNS is responsible for the "rest-and-digest" response.

    Anatomy of the Sympathetic Nervous System

    • Preganglionic sympathetic neurons originate from the spinal cord (T1-L2).
    • Sympathetic neurons synapse with ganglia, either paravertebral (chain of ganglia alongside the vertebral column), prevertebral (unpaired ganglia anterior to vertebral column), or the adrenal medulla (within the adrenal gland).
    • The adrenal medulla directly secretes catecholamines into the bloodstream.
    • Preganglionic fibers release acetylcholine at their synapse with postganglionic neurons, which release norepinephrine except for sweat glands, which release acetylcholine.

    Specific Sympathetic Ganglia

    • Stellate ganglia provide sympathetic innervation to the head, neck, and upper extremities.
    • Celiac plexus provides sympathetic and sensory innervation to the stomach, liver, spleen, pancreas, kidney, and GI tract.

    Anatomy and Function of the Parasympathetic Nervous System

    • Parasympathetic neurons originate from cranial nerves III, VII, IX, X, and sacral segments 2-4.
    • The vagus nerve carries approximately 75% of PNS traffic.
    • Parasympathetic neurons release acetylcholine at their synapses with postganglionic neurons, which also release acetylcholine.

    Adrenergic Receptors

    • There are alpha-1 (α1), alpha-2 (α2), beta-1 (β1), and beta-2 (β2) adrenergic receptors.
    • α1, β1, and β2 receptors are postsynaptic while α2 receptors are presynaptic.
    • Stimulation of α2 receptors inhibits NE release.

    Catecholamines

    • Catecholamines are monoamines that stimulate adrenergic nerve terminals.
    • Natural catecholamines include norepinephrine, epinephrine, and dopamine.
    • Synthetic catecholamines include dobutamine and isoproterenol.

    Synthesis of Catecholamines

    • Tyrosine is converted to dopamine by tyrosine hydroxylase and aromatic l-amino acid decarboxylase.
    • Dopamine is converted to norepinephrine by dopamine β-hydroxylase.
    • Norepinephrine is converted to epinephrine by phenylethanolamine N-methyltransferase.

    Metabolism of Catecholamines

    • Catecholamines are metabolized by monoamine oxidase and catecholamine O-methyltransferase.
    • Metanephrine and normetanephrine are the main metabolites of epinephrine and norepinephrine, respectively.

    Acetylcholine Metabolism

    • Acetylcholine is metabolized by acetylcholinesterase (AChE).

    Cholinergic Crisis

    • Cholinergic crisis is caused by ACh accumulation and can be caused by AChE inhibitors.
    • Symptoms include bradycardia, salivation, lacrimation, urination, defecation, emesis, bronchoconstriction, blindness, and muscular paralysis.
    • Treatment involves atropine and intubation.

    Beta-Adrenergic Antagonists

    • Commonly used for hypertension, angina, and dysrhythmias.
    • β1-blockade decreases heart rate, contractility, cardiac output, and myocardial oxygen requirement.
    • β2-blockade leads to vasoconstriction of the peripheral vessels.

    Alpha-2 Agonists

    • α2 agonists inhibit adenylate cyclase and decrease sympathetic outflow.
    • Dexmedetomidine is commonly used in the perioperative setting for sedation, analgesia, and reducing heart rate, blood pressure, and anesthetic requirement.

    Muscarinic Antagonists

    • Glycopyrrolate is the most commonly administered muscarinic antagonist in the operating room to reverse neuromuscular blockade.

    Autonomic Dysfunction

    • Patients with autonomic dysfunction are at risk for severe hypotension and aspiration.

    Spinal Cord Injury and the Autonomic Nervous System

    • Spinal cord injury can cause various ANS problems, including autonomic reflexes becoming exaggerated.
    • Autonomic dysreflexia is a dramatic increase in blood pressure and decrease in heart rate, managed by vasodilators and deepening anesthesia.

    Pheochromocytoma

    • Pheochromocytoma is a catecholamine-secreting tumor that causes paroxysmal episodes of hypertension, tachycardia, headache, and diaphoresis.
    • Diagnosis is confirmed by detecting elevated levels of metanephrine and normetanephrine.

    Compliance of Blood Vessels

    • Arteries are less compliant (less able to expand) than veins.
    • Stiff arteries, often due to arteriosclerosis, can cause hypertension and decrease the physiological reserve for hemorrhage.

    Physiological Response to Hemorrhage

    • Increased sympathetic tone constricts veins, decreasing venous compliance and facilitating venous return.
    • Aging leads to reduced compliance and a decreased capacity for blood volume recruitment.

    Hemorrhage and Sympathetic Tone

    • Sympathetic tone increases during hemorrhage to maintain blood pressure and cardiac output, ultimately preserving oxygen delivery to tissues.
    • Increased sympathetic tone releases norepinephrine and epinephrine, which stimulate α1 adrenergic receptors on the arteries and veins.
    • Arteriole α1 receptor stimulation increases systemic vascular resistance (SVR).
    • Venous α1 receptor stimulation decreases venous compliance, enhancing venous return and maintaining preload and cardiac output.
    • Catecholamines also increase heart rate (chronotropy) and contractility (inotropy) to maintain cardiac output.
    • Younger patients have greater physiological reserve and tolerate larger blood losses before experiencing vital sign abnormalities.
    • Older patients have diminished reserve due to atherosclerosis, decreased cardiac contractility, and medications like β-blockers.

    Heart Structure and Function

    • The heart, a muscular organ, generates a pressure gradient to drive nutrient and oxygen-rich blood delivery.
    • It consists of four chambers: two atria and two ventricles.
    • The heart is divided into right and left sides, with one-way pressure-regulated valves separating each chamber.

    Lung Volumes and Capacities

    • Tidal volume (TV): Volume of gas inspired and passively expired with normal breathing.
    • Expiratory reserve volume (ERV): Maximum volume of gas exhaled from rest.
    • Residual volume (RV): Gas remaining in the lungs after maximum exhalation.
    • Functional residual capacity (FRC): ERV + RV.
    • Inspiratory reserve volume (IRV): Maximum volume inhaled above TV.
    • Inspiratory capacity (IC): IRV + TV.
    • Vital capacity (VC): IRV + TV + ERV.
    • Total lung capacity (TLC): IRV + TV + ERV + RV.

    Body Water Compartments

    • Total body water comprises approximately 60% of body weight.
    • Intracellular fluid compartment holds two-thirds (40% of body weight).
    • Extracellular compartment holds one-third (20% of body weight).
    • Interstitial fluid constitutes three-quarters of extracellular fluid (15% of body weight).
    • Plasma volume comprises one-quarter of extracellular fluid (5% of body weight).
    • This can be remembered as the "20-40-60" rule: 20% extracellular, 40% intracellular, 60% total body water.

    Fluid Distribution Dynamics

    • Sterling's principle describes filtration between the intravascular and interstitial space.
    • The endothelial glycocalyx plays a significant role in fluid transfer, suggesting filtration occurs throughout the capillary bed.
    • Reabsorption from the interstitial space may not occur.
    • Net filtration is governed by the endothelial glycocalyx, endothelial basement membrane, and extracellular matrix.

    Serum Osmolarity

    • Normal serum osmolarity ranges between 285 and 305 mOsm/L.
    • A quick estimate can be obtained by doubling the sodium concentration.
    • Osmolarity can be calculated using a specific equation that accounts for sodium, glucose, and blood urea nitrogen (BUN) concentrations.

    Body Water and Tonicity Regulation

    • Antidiuretic hormone (ADH), also called vasopressin, is the primary mechanism of body water and tonicity regulation.
    • It increases aquaporin channel expression in the distal convoluted tubule and collecting duct, increasing tubular permeability to water.
    • This results in increased free water resorption and urine concentration.
    • Stimuli for ADH release include:
      • Hypothalamic osmoreceptors: Respond to hyperosmolarity.
      • Hypothalamic thirst center neurons: Regulate conscious water desire in response to hyperosmolarity.
      • Aortic baroreceptors and left atrial stretch receptors: Respond to hypotension and hypovolemia, respectively.
      • Increased sympathetic tone: From stress, surgery, or critical illness.
    • Hypovolemia and hypotension take precedence over osmolarity, leading to ADH secretion to maintain volume at the expense of osmolarity.

    ADH Synthesis

    • ADH is synthesized in the supraoptic and paraventricular nuclei of the hypothalamus.
    • It's transported to the posterior pituitary gland in secretory granules, where it is stored and released in response to hypothalamic stimuli.
    • ADH-producing neurons receive innervation from osmoreceptors and baroreceptors.

    ADH Release Stimuli and Inhibitors

    • Stimuli: Normal physiological states (hyperosmolarity, hypovolemia, upright position, β-adrenergic stimulation, pain, emotional stress, cholinergic stimulation), abnormal physiological states (hemorrhagic shock, hyperthermia, increased intracranial pressure, positive airway pressure, metabolic and respiratory acidosis), medications (morphine, nicotine, barbiturates, tricyclic antidepressants, chlorpropamide).
    • Inhibitors: Normal physiological states (hypoosmolarity, hypervolemia, supine position, α-adrenergic stimulation), abnormal physiological states (excess water intake, hypothermia), medications (ethanol, atropine, phenytoin, glucocorticoids, chlorpromazine).

    Diabetes Insipidus (DI)

    • DI is characterized by impaired ADH release (neurogenic DI) or renal resistance to ADH (nephrogenic DI).
    • It leads to large volumes of dilute urine, resulting in dehydration, hypernatremia, and serum hyperosmolarity.
    • Diagnosis involves cautious fluid restriction, plasma ADH measurements, and intravenous desmopressin (DDAVP) administration.

    Causes of DI

    • Neurogenic DI: Familial (autosomal-dominant), acquired (idiopathic, craniofacial and basilar skull fractures, pituitary tumors, lymphoma, metastasis, granuloma, central nervous system infections, Sheehan syndrome, hypoxic brain injury, brain herniation, brain death, pituitary surgery).
    • Neprogenic DI: Familial (X-linked recessive), acquired (pyelonephritis, postrenal obstruction, sickle cell disease and trait, amyloidosis, hypokalemia, hypercalcemia, sarcoidosis, lithium).

    Management of Central DI

    • ADH preparations: DDAVP (2 to 4 mcg intravenously every 2 to 4 hours) or vasopressin (titrated to urine output up to 2.4 units/h).
    • Hypotonic maintenance fluids: Dextrose 5% to replace free water deficit.
    • Avoid isotonic fluids: Normal saline (NS) can increase serum osmolarity.
    • Thiazide diuretics or chlorpropamide: May be used for incomplete DI.
    • Frequent monitoring: Plasma and urine osmolarity, urine output measurements.

    Syndrome of Inappropriate ADH (SIADH)

    • Characterized by serum hypotonicity due to nonosmotic ADH release, inhibiting renal water excretion.
    • Diagnostic criteria:
      • Euvolemia or hypervolemia.
      • Inappropriately concentrated urine (plasma osmolarity < urine osmolarity).
      • Normal renal, cardiac, hepatic, adrenal, and thyroid function.

    Management of SIADH

    • Primary therapy: Water restriction, often sufficient for asymptomatic hyponatremia.
    • Chronic SIADH: Demeclocycline (blocks ADH-mediated water resorption) or vaptans (ADH receptor antagonists).
    • Severe symptomatic hyponatremia: Intensive care unit admission, hypertonic saline.
    • Hyponatremia: Can lead to cerebral edema, increased intracranial pressure, and potentially fatal outcomes.

    Causes of SIADH

    • Central nervous system events: Acute intracranial hypertension, trauma, tumors, meningitis, subarachnoid hemorrhage.
    • Pulmonary causes: Tuberculosis, pneumonia, asthma, bronchiectasis, hypoxemia, hypercarbia, positive-pressure ventilation.
    • Malignancies: ADH-like compound production.
    • Adrenal insufficiency and hypothyroidism.

    Stress-Induced Hyponatremia

    • Stressful situations (surgery, critical illness) increase sympathetic tone, facilitating ADH release and activating the renin-angiotensin-aldosterone system.
    • This leads to free water reabsorption, decreasing urine output despite normal volume status.
    • It can result in mild dilutional hyponatremia, termed stress-induced hyponatremia.
    • Urine output is a poor indicator of intraoperative volume status.
    • Low urine output should not be ignored as it can indicate acute kidney injury, a predictor of perioperative mortality.

    Aldosterone

    • Controls sodium excretion.
    • Renin is released by the juxtaglomerular cells of the kidney in response to decreased renal or systemic arterial blood pressure, hypovolemia, and/or hyponatremia.
    • Renin converts angiotensinogen to angiotensin I, which is then converted to angiotensin II by angiotensin-converting enzyme.
    • Angiotensin II stimulates aldosterone release from the adrenal cortex.
    • Additional actions of angiotensin II include systemic vasoconstriction and ADH release.
    • Aldosterone acts on the distal renal tubules and collecting ducts to reabsorb sodium and excrete potassium, resulting in net fluid retention.
    • Stimuli for aldosterone release include hyperkalemia, increased adrenocorticotropic hormone levels, and increased sympathetic tone.

    Perioperative Fluid Status Derangements

    • Preoperative hypovolemia: Can be caused by bowel prep, active blood loss, or inflammatory processes.
    • Fasting before elective procedure: Does not significantly contribute to hypovolemia, current evidence does not support routine intraoperative volume replacement.
    • Intraoperative factors: Anesthetic medications and procedures can cause venous and arterial vasodilation, leading to hypotension that may be mistaken for hypovolemia.
    • Procedure-related blood loss, evaporative losses, and third-spacing: More likely causes of perioperative hypovolemia.
    • Evidence-based volume resuscitation strategies are recommended for hypovolemia.

    Consequences of Intraoperative Hypovolemia/Hypervolemia

    • Hypovolemia: Common in perioperative period, can lead to decreased cardiac output, tissue perfusion, and shock.
    • Hypervolemia: Can contribute to pulmonary edema, bowel edema, wound edema, and dilution of coagulation factors.
    • Optimal volume resuscitation is crucial to avoid under- or overresuscitation.

    Contraction Alkalosis

    • Chloride depletion alkalosis, most often occurs with hypovolemia and hypochloremia.
    • Examples include patients on diuretics with salt restriction or upper gastrointestinal losses.
    • Bicarbonate is preferentially reabsorbed due to chloride depletion.
    • Aldosterone-mediated renal hydrogen secretion plays a role.
    • Treatment requires chloride and volume resuscitation.
    • Chloride supplementation alone can rapidly correct the acid-base disturbance despite remaining hypovolemia.
    • Volume without chloride supplementation will not address metabolic alkalosis despite euvolemia.

    Fluid Administration During Surgery

    • Application of non-quantifiable methods for insensible fluid loss and third-space fluid migration can lead to overresuscitation.
    • Arbitrary fluid administration increases the risk of hypervolemia and complications.
    • Restrictive fluid maintenance (3–5 mL/kg/h) has shown better outcomes than liberal resuscitation (10–12 mL/kg/h).
    • Fluid restriction is particularly important in patients undergoing thoracotomy and lung resections.
    • Dynamic measurements of volume status (pulse pressure variation, stroke volume variation) are used to predict fluid responsiveness and decrease inappropriate fluid administration.

    Crystalloid Solutions

    • Balanced salt solutions (Plasma-Lyte or Ringer's lactate) are used for fluid resuscitation as they have a tonicity and electrolyte composition more consistent with extracellular fluid losses than hypotonic solutions.
    • Hypotonic fluids (e.g., 0.45% NS) are used for maintenance in healthy patients, but isotonic or balanced salt solutions are recommended for hospitalized patients with acute illnesses to minimize hyponatremia risk.
    • Maintenance fluids often include 5% dextrose to prevent hypoglycemia.
    • Total parental nutrition is advised for patients with prolonged malnutrition.

    Isotonic Crystalloid Solutions

    • Normal saline (NS) has a pH of 5.5 and can be as low as 4.6 when stored in polyvinyl chloride (PVC) bags.
    • NS contains 154 mEq/L of both sodium and chloride which are both higher than plasma.
    • Lactated Ringer's (LR) and Plasma-Lyte have a pH closer to plasma (6.5 and 7.4 respectively) and contain more electrolytes including calcium, magnesium, and potassium.
    • LR contains lactate which is converted by the liver into bicarbonate.
    • Plasma-Lyte contains gluconate and acetate which are also converted by the liver into bicarbonate.

    Disadvantages of Normal Saline

    • NS can cause hyperchloremic metabolic acidosis with prolonged administration.
    • Balanced salt solutions (LR and Plasma-Lyte) better reflect the composition of extracellular fluid.
    • NS is often given in clinical practice because of its lack of potassium, but LR and Plasma-Lyte are safe to use in patients with end-stage renal disease (ESRD).
    • 0.45% NS with 1.5 ampules of sodium bicarbonate is another option for patients with ESRD.
    • LR and Plasma-Lyte should be avoided with blood transfusions due to the potential for clotting.

    Colloids vs. Crystalloids

    • Colloids have a longer intravascular half-life of 3–6 hours compared to crystalloids (20–40 minutes).
    • Colloids are not shown to improve outcomes compared to crystalloids.
    • Albumin can accumulate in the interstitial space during increased capillary permeability, pulling other fluids along and leading to edema.
    • Crystalloids are recommended over albumin for fluid resuscitation.

    Albumin

    • There are two albumin preparations: 5% albumin and 25% albumin solution.
    • Albumin is not suitable for volume replacement and is more expensive than crystalloid solutions.
    • Albumin may be considered for hypervolemic, volume-responsive patients.

    Hypertonic Saline

    • Hypertonic saline (usually 3% or 23%) has an osmolarity of 900 mOsm/L.
    • Hypertonic saline can be used to treat hyponatremia and elevated intracranial pressure (ICP).

    Third-Space Losses

    • Third-space losses are internal and occur when fluid is sequestered into a non-functional space.
    • These losses require further fluid infusions to maintain adequate intravascular volume.
    • Third-space fluids generally persist until the primary problem resolves.

    Hyponatremia

    • Hyponatremia can be classified based on the patient’s serum osmolality and volume status.
    • Causes of hyponatremia include diuretics, renal tubular acidosis, hypoaldosteronism, salt-wasting nephropathies, vomiting, diarrhea, syndrome of inappropriate antidiuretic hormone (SIADH), hypothyroidism, cortisol deficiency, and fluid overload from conditions like congestive heart failure, cirrhosis, and nephrotic syndrome.

    Acute Hyponatremia

    • Acute hyponatremia can occur during surgery from hypotonic fluids, sodium-poor irrigation solutions, and mannitol administration.
    • Symptoms of acute hyponatremia include nausea, vomiting, visual disturbances, muscle cramps, weakness, bradycardia, mental status changes, and seizures.
    • Mild hyponatremia (sodium ≥ 130 mEq/L) with no symptoms does not need to be treated prior to elective surgery.
    • Hyponatremia treatment depends on the severity of symptoms and rate of change. Fluid restriction, loop diuretics, and hypertonic saline may be indicated.
    • Rate of sodium correction should not exceed 0.5 mEq/L/h for asymptomatic patients and 10–12 mEq/L/day. If there is concern about osmotic demyelination syndrome, the rate can be decreased.
    • Osmotic demyelination syndrome is less likely to occur in patients whose initial sodium level is higher than 120 mEq/L.
    • Symptoms of osmotic demyelination syndrome typically develop 2–6 days after rapid sodium changes and include confusion, movement disorders, seizures, weakness, and myoclonic jerks.

    Hypernatremia

    • Hypernatremia is less common than hyponatremia and is always associated with hypertonicity.
    • Hypernatremia can be present with low, normal, or high total body sodium content.

    Hypernatremia

    • It's commonly caused by decreased free water access in elderly or debilitated patients with impaired thirst and oral intake.
    • Can also be caused by lack of antidiuretic hormone (central diabetes insipidus) or lack of response to antidiuretic hormone (nephrogenic diabetes insipidus).
    • Often iatrogenic in hospitalized patients caused by excess sodium intake through intravenous fluids, especially normal saline, or medications, like sodium bicarbonate or 3% sodium chloride.

    Hypernatremia in Anesthesia

    • Increases the minimal alveolar concentration for inhaled anesthetics.
    • Usually poses a challenge due to fluid deficits, requiring slow correction to prevent cellular edema.
    • Procedures involving significant resuscitation and fluid shifts increase the risk of rapid sodium changes.
    • Elective surgery should be delayed with serum sodium exceeding 150 mEq/L.

    Hypokalemia

    • Normal serum potassium concentration is 3.5 to 5.0 mEq/L.
    • Low serum potassium reflects significant total body potassium depletion.
    • Causes include gastrointestinal losses (diarrhea, laxative overuse, pseudoobstruction), renal losses (diuretics, renal tubular acidosis), transcellular shifts (β-adrenergic agonists, insulin, elevated serum pH), and inadequate intake.

    Hypokalemia Complications

    • Electrocardiogram abnormalities (ST segment and T wave depression, prolonged QT interval, U waves) and cardiac arrhythmias.
    • Impairs cardiac contractility, usually notable when potassium is below 3 mEq/L.
    • Patients taking digitalis, with preexisting arrhythmias or ischemic heart disease are more susceptible to even mild decreases.
    • Causes muscle weakness, including respiratory muscle weakness, and increases sensitivity to muscle relaxants.
    • Increases the risk of ileus and long-term damage to the kidneys.

    Hypokalemia Treatment

    • Total body potassium deficit is not accurately reflected by serum concentrations.
    • Rapid correction attempts are ineffective and can lead to cardiac arrest.
    • Patients without risk factors and not undergoing major thoracic, vascular, or cardiac procedures can tolerate hypokalemia to 3 mEq/L and possibly 2.5 mEq/L.

    Managing Hypokalemia

    • Each 10 mEq of potassium administered increases serum potassium by approximately 0.1 mEq/L (less accurate for patients with severe depletion, ongoing losses, or renal insufficiency).
    • Infusion limits are 20 mEq/h via a central line or 10 mEq/h via a peripheral line.
    • Injectable potassium chloride should never be given undiluted or as a bolus, and no more than 20 mEq should be connected to IV lines.
    • Mild and asymptomatic hypokalemia can be treated with oral potassium (40-60 mEq, 1-4 times daily, maximum 100 mEq/day).

    Hyperkalemia

    • Defined as serum potassium greater than 5.0 mEq/L, but symptoms typically develop at 5.5 mEq/L or higher.
    • Causes include increased intake, decreased excretion, and transcellular shifts due to low serum pH.
    • Increased intake is often iatrogenic (potassium supplementation or medications).
    • Increased potassium release from cells can cause hyperkalemia (trauma, rhabdomyolysis, hemolysis, tumor lysis, massive transfusion).
    • Decreased excretion is most common due to renal dysfunction (acute or chronic).

    Hyperkalemia and Succinylcholine

    • Routine succinylcholine administration increases serum potassium by approximately 0.5 mEq/L.
    • Should be avoided in patients with hyperkalemia and subpopulations susceptible to exaggerated potassium response (spinal cord/denervation injuries, stroke, head injuries, burns, rhabdomyolysis, intraabdominal infections, immobility).
    • Conservatively, avoid succinylcholine in patients with acute burns, stroke, or spinal cord injury after 24 hours.

    Hyperkalemia in Chronic Renal Failure

    • Hyperkalemia greater than 6 mEq/L should be corrected before elective procedures.
    • Dialysis is usually the preferred treatment, with intermittent hemodialysis preferred for significant or symptomatic hyperkalemia.

    Treating Acute Hyperkalemia

    • Cardiotoxicity is treated with intravenous calcium chloride or calcium gluconate.
    • Potassium can be shifted intracellularly with β-adrenergic stimulation (inhaled albuterol) and intravenous insulin (with dextrose supplementation).
    • Hyperventilation and sodium bicarbonate can be beneficial in acidemia.
    • Excretion can be achieved using diuretics, sodium polystyrene sulfonate (Kayexalate), and dialysis.
    • Intravenous fluids (normal saline) may be helpful in hypovolemic patients.

    Hypocalcemia Causes

    • Major causes include hypoparathyroidism, hyperphosphatemia, vitamin D deficiency, malabsorption, rapid blood transfusion (calcium chelation by citrate), pancreatitis, rhabdomyolysis, and fat embolism.
    • It's a concern after thyroidectomy if parathyroid tissue is removed, potentially leading to laryngeal spasms and stridor.

    Hypocalcemia Manifestations

    • Impairs cardiac contractility, resulting in hypotension.
    • QT prolongation is possible, but conduction abnormalities are less common than other electrolyte abnormalities.
    • Can cause tetany, perioral paresthesias, seizures, anxiety, and confusion.
    • Trousseau's sign (carpopedal spasm with blood pressure cuff inflation) and Chvostek's sign (facial muscle contraction with facial nerve tapping) may be present.

    Ionized Calcium in Hypocalcemia

    • Serum calcium is bound to proteins, primarily albumin.
    • Total serum calcium may not represent the ionized (free) calcium level which is clinically relevant.
    • Each 1 g/dL reduction in albumin lowers total calcium by 0.8 mg/dL but doesn't affect ionized calcium.
    • Affinity of calcium for albumin is higher in alkalosis, so ionized calcium may be decreased with elevated serum pH.

    Treating Hypocalcemia

    • Intravenous calcium chloride or calcium gluconate.
    • Always address the primary disturbance.
    • Calcium chloride provides more active calcium than gluconate.
    • Calcium gluconate is preferable if central access is unavailable due to less irritation and lower risk of tissue necrosis with extravasation.

    Magnesium Levels and Symptoms

    • Normal serum magnesium is 1.3 to 2.2 mEq/L.
    • Hypomagnesemia causes QT prolongation and can lead to torsades de pointes and other arrhythmias.
    • Other symptoms include muscle weakness, tremors, twitches, numbness, and paresthesias, as well as confusion, drowsiness, and seizures in severe cases.
    • Hypermagnesemia is uncommon, usually caused by renal dysfunction or excessive intake (iatrogenic, used therapeutically for preeclampsia and eclampsia).
    • Initial symptoms of magnesium toxicity occur at 4 to 6 mEq/L (nausea, headache, drowsiness, decreased reflexes).
    • As the magnesium level increases, patients develop muscle weakness, respiratory insufficiency/failure, absent reflexes, hypotension, bradycardia, and possible cardiac arrest.

    Hypomagnesemia in Anesthesia

    • Increasingly recognized in patients with gastrointestinal losses, malnutrition, alcoholism, and critical illness.
    • Often associated with hypokalemia and hypophosphatemia.
    • Hypokalemia is difficult to correct unless hypomagnesemia is also addressed.
    • Mechanism is not fully understood but may be due to magnesium deficiency exacerbating potassium excretion.
    • Patients with hypomagnesemia have increased susceptibility to muscle relaxants and may be weak after surgery (respiratory insufficiency possible).
    • They may have impaired cardiac contractility and dysrhythmias (torsades de pointes).
    • Patients undergoing massive resuscitation are also at risk and should receive magnesium chloride if dysrhythmias or refractory hypotension develop.

    Chloride and Hyperchloremia

    • Hyperchloremia is increasingly recognized after administration of 0.9% normal saline.
    • Patients undergoing prolonged surgeries, septic shock, or significant trauma are most at risk due to large-volume fluid resuscitation needs.
    • Hyperchloremia also causes nonanion gap metabolic acidosis.

    Electrolyte Key Points

    • Correcting electrolyte disturbances is challenging without addressing the underlying cause.
    • Emergent hypertonic saline treatment for hyponatremia is reserved for severe neurological symptoms.
    • Hypernatremia is often associated with fluid deficits, requiring careful correction to prevent cellular edema.
    • Hyperkalemia cardiotoxicity needs immediate treatment with intravenous calcium chloride or gluconate.
    • Patients receiving high volumes of fluid, especially normal saline, often develop hyperchloremia and nonanion gap metabolic acidosis.

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    Test your knowledge on the autonomic nervous system (ANS) and its components, including the sympathetic and parasympathetic nervous systems. This quiz covers the ANS's role in regulating physiological actions like homeostasis and its anatomy. Explore how the SNS and PNS interact and influence various bodily functions.

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