Unit 1 Combined

Q: Who initiated the use of anesthesia support personnel in the late 1930s in England, and who was enlisted to assist?

Sir Robert Macintosh initiated it, enlisting Richard Salt.

Q: For most of the 20th century, how were anesthesia technicians typically trained?

They typically underwent on-the-job training (OJT) with no standardized educational programs.

Q: When and where was the American Society of Anesthesia Technologists and Technicians (ASATT) formed?

ASATT was formed in October 1989 in New Orleans, coinciding with the annual American Society of Anesthesiologists (ASA) meeting.

Q: What was ASATT's mission upon its formation?

ASATT's mission was to legitimize anesthesia technology as a profession, advocate for formalized training, and foster educational and professional support.

Q: When was the first written certification exam for anesthesia technicians administered by ASATT?

The first written certification exam for anesthesia technicians was administered in 1996.

Q: When did ASATT launch the first technologist-level exam, and when did it return after an initial hiatus?

ASATT launched the first technologist-level exam in 2001. After an initial hiatus due to waning interest, it returned in 2006.

Q: When did the Commission on Accreditation of Allied Health Education Programs (CAAHEP) officially recognize anesthesia technology as an allied health discipline?

CAAHEP officially recognized anesthesia technology as an allied health discipline in 2010.

Q: Which exam was retired in 2015, focusing new entries into the technologist path?

The Certified Anesthesia Technician (Cer.A.T.) exam was retired in 2015.

Q: Which organizations endorse both technician and technologist credentials?

Both technician and technologist credentials are endorsed by the American Society of Anesthesiologists (ASA) and the American Association of Nurse Anesthetists (AANA).

Q: Who comprises the ASATT Item Writers Committee for certification exams?

The committee includes anesthesiologists, CRNAs, certified technologists, corporate representatives, educators, and AMP professionals.

Q: What are the six certification domains for ASATT exams?

The six domains are: Equipment, Instrumentation, and Technology; Basic Sciences; Pharmacology; Basic and Advanced Principles of Anesthesia; and Professional Aspects.

Q: What are the recertification requirements for Certified Anesthesia Technicians (Cer.A.T.s), even though the exam is retired?

Current Cer.A.T.s must recertify every two years with 20 continuing education hours (CEHs) relevant to their certification.

Q: What are the eligibility requirements for the Certified Technologist Exam (Cer.A.T.T.)?

It requires graduation from an ASATT- or CAAHEP-accredited program, submission of an official transcript, and 30 CEHs for biannual recertification. The certification period runs for two full years post-requirements.

Q: What certifications are mandatory for continued certification for both technicians and technologists?

Proof of current BCLS (Basic Cardiac Life Support) and ACLS (Advanced Cardiac Life Support) certification is mandatory.

Q: What is the "Advancement Program" designed for?

The "Advancement Program" provides a clinical and didactic pathway for technicians seeking technologist certification, requiring both educational credits and employment benchmarks.

Q: What are the requirements for provisional certification if a certification has lapsed within 30 days?

Provisional certification is possible if requisite applications and remediation fees are submitted, and lapsed personnel must accrue more CE hours within a strict timeline.

Q: What are the requirements for refresher programs for techs/technologists returning after an absence of 2–5 years?

They require 40 CE hours, documentation of 240 hours of clinical work, and current BCLS/ACLS. Candidates may retake the exam with up to three attempts in one year.

Q: What type of educational programs are now required for new entrants pursuing certification since CAAHEP's 2010 recognition?

Accredited college-based programs are required, and OJT pathways are being phased out.

Q: What are the benefits and impact of certification for anesthesia technologists/technicians?

Certification demonstrates ongoing education, compliance with the latest clinical standards and technology, participation in quality assurance and regulatory adherence, and can lead to improved pay or advancement opportunities. Certified personnel play critical roles in patient safety and operating room efficiency.

Q: What is ASATT's motto and what does it underscore?

ASATT's motto is "Assisting with Safe Anesthesia Today and Tomorrow," underscoring the ongoing mission of readiness for both routine and emergent clinical scenarios.

Q: What is pivotal for both quality assurance and reducing costs/variability associated with OJT?

CAAHEP accreditation is pivotal for both quality assurance and for reducing the costs and variability associated with OJT.

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Flashcards for "Chapt 10 Summary.pdf"

Q: According to the Brønsted-Lowry Theory, how are acids and bases defined?

Acids donate hydrogen ions (H⁺) in water, while bases accept H⁺.

Q: What is the formula for pH, and what does a low pH indicate?

pH = -log₁₀[H⁺]. A low pH indicates an acidic solution with a high [H⁺] concentration.

Q: What is the optimal human arterial pH, and why is venous pH typically lower?

The optimal human arterial pH is 7.4, which is slightly alkaline. Venous pH is lower due to more acidic waste products being carried for elimination.

Q: What are the clinical consequences of acidosis in the cardiovascular system?

At pH 7.2, heart contractility falters. At 7.1, the heart and vasculature are less responsive to catecholamines, making blood pressure harder to manage during surgery. Acidosis also triggers peripheral arterial dilation, pulmonary artery constriction, and causes potassium to shift out of cells.

Q: What are the clinical consequences of alkalosis?

Alkalosis causes neuromuscular irritability, arrhythmias, muscle cramps, and can be life-threatening.

Q: What are the main endogenous sources of acids in the body?

Protein metabolism produces phosphoric and sulfuric acids, while carbohydrate/fat metabolism produces CO₂, which forms carbonic acid (H₂CO₃).

Q: How is CO₂ transported in the body?

CO₂ is transported as dissolved CO₂, as HCO₃⁻ (bicarbonate) after reacting with H₂O, and bound to hemoglobin (carbaminohemoglobin).

Q: What is Respiratory Acidosis, and what are its common causes?

Respiratory Acidosis is the accumulation of CO₂ (hypoventilation) due to opioid overdose, anesthetic narcosis, mechanical underventilation, neuromuscular weakness, or lung disease.

Q: What is Respiratory Alkalosis, and what are its common causes?

Respiratory Alkalosis is the excess removal of CO₂ (hyperventilation) due to anxiety, liver failure, pregnancy, aspirin overdose, or surgical hyperventilation.

Q: What happens when there is low oxygen in the body in terms of acid-base balance?

Low O₂ leads to anaerobic glycolysis, which results in lactic acid accumulation and metabolic (lactic) acidosis.

Q: What three primary values does an Arterial Blood Gas (ABG) yield, and what value is calculated?

An ABG yields pH, pCO₂, and pO₂. [HCO₃⁻] is calculated (not measured directly).

Q: What are the normal ranges for pH, pCO₂, and HCO₃⁻ in ABG interpretation?

pH: 7.35–7.45;

pCO₂: 35–45 mmHg;

pO2: 80-100 mmHg

HCO₃⁻: 22–26 mEq/L

Q: What are the main buffer systems in the body that help maintain acid-base balance?

The main buffer systems include plasma HCO₃⁻ (most important), hemoglobin, bone, proteins, and phosphate.

Q: What is the Anion Gap, and how is it used to classify metabolic acidosis?

The anion gap is calculated as (Na⁺ - [Cl⁻ + HCO₃⁻]), with a normal range of 8–12. It classifies metabolic acidosis as either non-anion-gap (HCO₃⁻ lost/replaced by Cl⁻) or anion-gap (acid introduced whose anion is not measured, e.g., lactate, ketoacids).

Q: What are common causes of metabolic alkalosis?

Metabolic alkalosis is caused by the loss of H⁺ (e.g., vomiting, NG suction, diuretic-induced fluid losses) or excess mineralocorticoids (aldosterone).

Q: What are the body's two primary compensatory mechanisms for acid-base disturbances, and what are their respective speeds and power?

The lungs provide immediate, fast but limited compensation by changing respiratory rate/depth. The kidneys provide slower (hours to days), but more powerful adjustment of acid/base excretion and reabsorption.

Q: How do peripheral and central chemoreceptors contribute to acid-base balance?

Peripheral chemoreceptors (carotid, aortic bodies) sense low O₂ and drive up ventilation. Central chemoreceptors (medulla) sense changes in CO₂ and direct breathing to maintain pH homeostasis.

Q: Why is pulse oximetry, while standard, insufficient for revealing acid-base status or CO₂ levels?

Pulse oximetry only measures oxygen saturation and does not provide information about acid-base status or CO₂ levels, unlike ABG.

Q: Which organ does NOT participate in acid-base regulation, according to the sources?

The gallbladder does not participate in acid-base regulation; the lungs, kidneys, GI, and CNS do.

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Flashcards for "Chapt 11 Summary.pdf"

Q: What two main structures comprise the Central Nervous System (CNS)?

The brain and spinal cord comprise the CNS.

Q: What are the two main components of the cerebral hemispheres, and what are their primary functions?

The cerebral hemispheres consist of gray matter (cerebral cortex, site of cell bodies, synaptic activity, integration centers) and white matter (myelinated axonal tracts interconnecting brain regions).

Q: What are the four principal lobes of the cerebral hemispheres, and what is the primary function of the occipital lobe?

The four lobes are Occipital, Temporal, Parietal, and Frontal. The Occipital Lobe is specialized for visual processing.

Q: Which lobe is responsible for auditory perception, memory formation, and aspects of language processing (Wernicke's area)?

The Temporal Lobe is key for auditory perception, memory formation (hippocampus), and aspects of language processing (Wernicke’s area).

Q: What are the primary functions of the Parietal Lobe?

The Parietal Lobe is responsible for somatosensation (touch, pressure, pain), spatial relationships, and the interface between sensory and language comprehension.

Q: Which lobe governs executive functions, decision-making, planning, attention, social judgment, and voluntary motor control, including Broca's area?

The Frontal Lobe governs these functions and contains Broca's area (speech production).

QQ: What is the primary function of the Thalamus?

The Thalamus is the sensory “relay station”—all sensory (except olfactory) signals pass through it for processing and routing.

Q: What are the key functions of the Hypothalamus?

The Hypothalamus governs hunger, thirst, temperature, circadian rhythms, emotional behavior, and hormone release via the pituitary gland.

Q: Where is the Cerebellum located, and what are its primary roles?

The Cerebellum is located posteriorly, under the occipital lobe. It coordinates smooth, efficient voluntary movement, maintains posture, balance, and procedural ("muscle") memory.

QQ: What are the three components of the Brainstem, and what vital functions does it orchestrate?

The Brainstem includes the midbrain, pons, and medulla oblongata. It orchestrates autonomic/vital functions such as breathing and heart rate.

QQ: Name the three layers of the Meninges, from outermost to innermost.

The three layers are dura mater (tough, outermost), arachnoid mater (weblike, contains subarachnoid space filled with CSF), and pia mater (delicate, adherent to brain surface).

Q: What are the functions of Cerebrospinal Fluid (CSF)?

CSF circulates in ventricles and subarachnoid space, acting as a shock absorber, facilitating waste removal, and maintaining consistent intracranial pressure (ICP).

Q: How does anesthesia affect Intracranial Pressure (ICP)?

Inhaled anesthetics cause vasodilation, leading to increased cerebral blood flow and potential ICP elevation. Neuroanesthesia often utilizes IV anesthetics to minimize this.

Q: How do changes in PaCO₂ affect ICP?

Low PaCO₂ (from hyperventilation) causes cerebral vasoconstriction, which decreases ICP. Increased PaCO₂ (hypoventilation) causes vasodilation, which increases ICP.

QQ: Where does the spinal cord originate and terminate?

The spinal cord originates just below the brainstem, terminating near the L1 vertebra.

Q: What is the difference between Spinal (Subarachnoid) Anesthesia and Epidural Anesthesia in terms of needle placement?

In Spinal Anesthesia, the needle traverses the ligamentum flavum and dura/arachnoid into the CSF. In Epidural Anesthesia, the needle stops outside the dura.

QQ: What are the four main components of a neuron and their functions?

A neuron has a Soma (cell body), Dendrites (receive information), an Axon (transmits action potentials), and Axon Terminals (synaptic signaling).

Q: What is the function of Myelin, and which cells produce it in the CNS and PNS?

Myelin is a lipid-rich sheath that insulates axons to facilitate rapid signal conduction (saltatory conduction). It is produced by oligodendrocytes in the CNS and Schwann cells in the PNS.

Q: Which two areas of the brain are primarily responsible for language, specifically speech production and comprehension?

Broca’s area (speech production) is in the left frontal lobe, and Wernicke’s area (comprehension) is in the left temporal lobe.

Q: What are the key effects of General Anesthetics on the CNS?

General anesthetics induce unconsciousness, analgesia, amnesia, and muscle relaxation.

QQ: What is the Chemoreceptor Trigger Zone (CTZ), and where is it located?

The CTZ is a centrally coordinated area in the medulla responsible for vomiting (emesis).

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Flashcards for "Chapt 12 Summary.pdf"

Q: What are the two main subdivisions of the Peripheral Nervous System (PNS)?

The PNS is divided into the Autonomic Nervous System (ANS) and the Sensory-Somatic Nervous System.

Q: How many pairs of cranial nerves and spinal nerves comprise the sensory-somatic nervous system?

It comprises 12 cranial nerve pairs and 31 spinal nerve pairs.

Q: What is the difference between afferent and efferent nerves?

Afferent nerves transmit sensory data from peripheral receptors towards the CNS. Efferent nerves send motor signals from the CNS out to effect voluntary muscle contraction.

Q: Describe the three layers of connective tissue surrounding a peripheral nerve, from innermost to outermost.

Endoneurium surrounds individual axons, perineurium groups axons into fascicles, and epineurium bundles fascicles into a nerve.

QQ: What maintains the resting membrane potential of a neuron?

The resting membrane potential is maintained by a sodium-potassium pump (active transport), resulting in high K+ inside and high Na+ outside, with the inside being negatively charged.

QQ: What causes depolarization during an action potential in a neuron?

An action potential initiates when stimulated, opening Na+ channels and allowing an inward surge of Na+, making the interior positive compared to the exterior.

QQ: What is saltatory conduction, and how does it affect nerve signal speed?

Saltatory conduction is when action potentials "jump" between nodes of Ranvier on myelinated axons, greatly increasing conduction speed.

Q: Why are neurons uniquely susceptible to ischemia?

Neurons are uniquely susceptible to ischemia because of their high metabolic requirements.

QQ: How do local anesthetics work at a molecular level to block nerve signals?

Local anesthetics block voltage-gated Na+ channels, halting action potential propagation and causing regional loss of sensation or muscle control.

QQ: What are the three structural components common to all local anesthetics?

All local anesthetics share an aromatic ring (lipophilic), an intermediate chain (determines amide or ester class), and an amine group (hydrophilic).

Q: How does a local anesthetic's pKa affect its onset of action?

The closer the pKa is to physiological pH (7.4), the greater the proportion of the drug that is nonionized. The nonionized form can cross cell membranes faster, leading to a faster onset of action.

QQ: Provide an example of a local anesthetic with a fast onset and one with a slower onset, relating them to their pKa values.

Lidocaine (pKa 7.8) has a faster onset. Bupivacaine (pKa 8.1) has a slower onset.

QQ: Which class of local anesthetics is more likely to provoke allergic reactions?

Ester local anesthetics more often provoke allergic reactions.

QQ: What are the progressive symptoms of systemic local anesthetic toxicity?

Symptoms progress from CNS excitement (metallic taste, numbness, tinnitus, light-headedness), then to CNS depression (seizures, coma), and finally to cardiovascular collapse (arrhythmias, cardiac arrest).

QQ: Which local anesthetic is highlighted as having the highest cardiotoxicity, especially with inadvertent intravascular injection?

Bupivacaine is highlighted as having the highest cardiotoxicity.

QQ: Why is proper patient positioning critical during surgical procedures in relation to the PNS?

The PNS is metabolically active; compressive or ischemic injury can lead to deficits, so proper patient positioning is critical to prevent perioperative nerve injury.

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Flashcards for "Chapt 13 Summary.pdf"

QQ: What is the Autonomic Nervous System (ANS) responsible for?

The ANS is a branch of the peripheral nervous system responsible for the involuntary regulation of visceral (internal organ) functions, such as heart rate, digestion, and respiration.

Q: What are the two main subdivisions of the ANS and their primary roles?

The Sympathetic Nervous System (SNS) prepares the body for stress ("fight-or-flight"). The Parasympathetic Nervous System (PNS) restores the body to rest ("rest-and-restore" or "rest-and-digest").

QQ: How do the neuronal pathways of the somatic and autonomic systems differ?

The somatic system uses direct, one-neuron pathways. The ANS uses two-neuron pathways (preganglionic and postganglionic) separated by a ganglion.

QQ: What are the exclusive effector targets of the ANS?

The ANS exclusively targets smooth muscle, cardiac muscle, and secretory glands.

QQ: Where do preganglionic fibers of the sympathetic division originate, giving it its designation?

Preganglionic fibers of the sympathetic division arise from the thoracic (T1-T12) and upper lumbar (L1–L3) spinal cord, hence its "thoracolumbar" designation.

QQ: What is the adrenal medulla considered in relation to the sympathetic nervous system?

The adrenal medulla is considered a modified sympathetic ganglion, where preganglionic neurons synapse directly with chromaffin cells to release catecholamines (epinephrine and norepinephrine).

Q: Where do preganglionic neurons of the parasympathetic division originate, giving it its designation?

Preganglionic neurons of the parasympathetic division begin with cranial nerves III, VII, IX, and X, and sacral spinal nerves, earning it the "craniosacral" designation.

QQ: What is the major role of the vagus nerve (Cranial Nerve X) in parasympathetic innervation?

The vagus nerve supplies almost all thoracic and abdominal viscera, regulating heart rate, bronchomotor tone, and GI tract functions.

QQ: Which neurotransmitter is always released by preganglionic fibers in both the SNS and PNS?

Acetylcholine is always released by preganglionic fibers.

QQ: What is the primary postganglionic neurotransmitter of the SNS, with one exception?

Norepinephrine is the primary postganglionic neurotransmitter, except for sympathetic fibers innervating sweat glands, which use acetylcholine.

QQ: Name the two types of cholinergic receptors and where they are found.

Nicotinic receptors (always excitatory) are found at all autonomic ganglia. Muscarinic receptors (excitatory or inhibitory) are found on effector tissues of the PNS.

QQ: What are the main effects of stimulating α1 and β1 adrenergic receptors?

α1 stimulation causes vasoconstriction and increased BP. β1 stimulation increases heart rate and contractility.

QQ: What are the main effects of stimulating β2 adrenergic receptors?

β2 stimulation causes bronchodilation, vasodilation, and increased glucose.

QQ: List three sympathetic effects on the heart, blood vessels, and GI tract.

Sympathetic stimulation causes increased heart rate and force, vasoconstriction (increased BP), and decreased GI motility and secretions.

QQ: List three parasympathetic effects on the heart, GI tract, and eyes.

Parasympathetic stimulation causes decreased heart rate and force, increased GI motility and secretions, and pupil constriction (miosis).