LSU CRNA Interview 2025

Sympathetic nervous system

The sympathetic nervous system (SNS) is responsible for the "fight or flight" response—preparing the body to react to stress or emergencies.

1.) Event occurs and in your spinal cord (thoracolumbar T1-L2) has preganglionic neurons that releases acetylcholine (ACh). ACh binds to nicotinic receptors on the postganglionic neuron.

2.) Most postganglionic sympathetic neurons release:

-Norepinephrine (NE) (primary)

-Some specialized neurons release epinephrine (Epi) (mostly from adrenal medulla)

These neurotransmitters act on adrenergic receptors (GPCRs: G -protein-coupled receptor) on target cells. When norepinephrine or epinephrine binds to the adrenergic receptor: The receptor changes shape and activates a G-protein inside the cell. The G-protein triggers chemical signals inside the cell (like cAMP or calcium).

-α1 (smooth muscle)Gq↑ IP₃/DAG → ↑ Ca²⁺: Stimulates Smooth muscle, blood vessels, pupils (dilate) , bladder causes contraction (vasoconstriction). Nor > Epi, Increase SVR

-α2 (presynaptic neurons, CNS)Gi↓ cAMP Inhibits NE release (negative feedback)

-β1 (heart, kidney)Gs↑ cAMP↑ Heart rate, ↑ contractility, ↑ renin which releases angiotensin 2, aldosterone and ADH these increase blood volume and BP

-β2 (lungs, vessels, GI)Gs↑ cAMPSmooth muscle relaxation (bronchodilation, vasodilation), Epi > Nore, also acts on skeletal muscles blood vessels

-β3 (fat tissue)Gs↑ cAMPLipolysis (fat breakdown)

Sympathetic Adrenal Response

Preganglionic sympathetic fibers directly stimulate adrenal medulla

Adrenal chromaffin cells (modified postganglionic neurons) release:

~80% epinephrine

~20% norepinephrine

These hormones enter the bloodstream and act on distant adrenergic receptors, causing systemic effects.

Parasympathetic Nervous system

Parasympathetic Nervous System (PNS)

The parasympathetic nervous system is one branch of the autonomic nervous system (ANS), which controls involuntary bodily functions. The PNS is often described by the phrase:"Rest and digest"

🔍 Main Functions of the Parasympathetic Nervous System:

SystemEffect

-Heart↓ Heart rate (bradycardia)

-LungsBronchoconstriction, ↑ secretions

-GI tract↑ Motility, ↑ digestive secretions

-Eyes Pupil constriction (miosis), ↑ tear production

-BladderPromotes urination (detrusor contraction, sphincter relaxation)

-Salivary glands↑ Saliva production (watery saliva)

-Liver↑ Glycogen synthesis

-Sexual organs Erection (via vasodilation)

⚙️ Neurotransmitters & Receptors:

Neurotransmitter (ACh)Nicotinic (N) Ganglia (between pre- and postganglionic neurons)

Acetylcholine (ACh)Muscarinic (M1-M5) Target organs (heart, lungs, GI, etc.)

Most parasympathetic actions are mediated via muscarinic receptors (M2, M3):

M2 = Heart (↓ HR, ↓ contractility)

M3 = Smooth muscle (bronchoconstriction, ↑ secretions, bladder contraction)

Anatomy of the PNS:

Origin: Craniosacral outflow

Cranial nerves: III (oculomotor), VII (facial), IX (glossopharyngeal), X (vagus)

Sacral nerves: S2-S4 (pelvic nerves)

Long preganglionic fibers, short postganglionic fibers

Ganglia located near or inside target organs

Clinical Relevance:

Cholinergic drugs (e.g., bethanechol, pilocarpine) stimulate PNS activity.

Anticholinergics (e.g., atropine, glycopyrrolate) block PNS activity.

Overstimulation (e.g., organophosphate poisoning) can cause:

Bradycardia

Bronchospasm

Salivation, Lacrimation, Urination, Diarrhea (SLUD symptoms)

what is a catecholamine neurotransmitter?

Catecholamine Neurotransmitter

A catecholamine is a type of neurotransmitter, specifically a monoamine, that plays a vital role in the nervous system and body functions. These molecules, including dopamine, norepinephrine, and epinephrine, are synthesized from the amino acid tyrosine.

Catecholamines act as both neurotransmitters in the brain and hormones in the body, influencing a wide range of functions like mood, movement, and the body's stress response.

1.) Tyrosine → L-DOPA

Enzyme: Tyrosine hydroxylase Rate-limiting step

What happens? A hydroxyl group is added to tyrosine.

Where? Neurons and adrenal medulla.

2. L-DOPA → Dopamine

Enzyme: DOPA decarboxylase

What happens? A carboxyl group is removed.

✅ Now you have dopamine, which is:

A neurotransmitter in the brain,

A precursor to the next two catecholamines.

3. Dopamine → Norepinephrine

Enzyme: Dopamine β-hydroxylase

What happens? A hydroxyl group is added to the β-carbon.

✅ Now you have norepinephrine (neurotransmitter and hormone).

4. Norepinephrine → Epinephrine

Enzyme: Phenylethanolamine N-methyltransferase (PNMT)

What happens? A methyl group is added to the amine.

✅ Now you have epinephrine, mostly made in the adrenal medulla under the influence of cortisol.

What is an agonist?

These are drugs that bind to and activate certain receptors in the body, mimicking the action of a naturally occurring substance.

What is an antagonist?

These drugs bind to receptors but do not activate them. Instead, they block or dampen the normal response by preventing other molecules, like hormones or neurotransmitters, from binding to the receptor.

Norepinephrine: What receptors?

Norepinephrine Receptors

Alpha 1: Vasoconstrictions, Increase SVR, PVR, BP

Beta 1: increase HR (chronotropic effect) and contractility (inotropic effect), Increases CO which increases BP

Norepinephrine

Norepinephrine

MOA: it is a catecholamine with both alpha-adrenergic and beta-adrenergic agonist effects, primary action is vasoconstriction through alpha 1 receptor activation. This results in Increase PVR, SVR, and BP

B1: Increases HR (Chorotropic effect); increases contractility (Inotropic effect)

It is also synthesized both endogenously and for pharmaceutical use. Endogenously produced in the adrenal medulla and some neurons from the amnio acid tyrosine converted to L-Dopa.

1st line for septic shock, increase SBP and DBP with less increase in heart rate. Dose: 0.05 to 0.1 mcg/kg/min

Epinephrine

Mechanism of Action for Epinephrine

Epinephrine (also called adrenaline) is a catecholamine that acts as both a hormone and neurotransmitter. Its primary job is to help the body respond to stress, emergency, or "fight-or-flight" situations.

⚙️ How It Works — Step by Step

1. Binds to Adrenergic Receptors (GPCRs)

Epinephrine binds to adrenergic receptors on target cells.

There are several types of adrenergic receptors: a1, B1, and B2

These second messengers trigger cellular responses like muscle contraction, relaxation, increased heart rate, etc.

Dosage: 1mg Code push Q3 -5 min

IV drip: 1-20mcg/min

3. Tissue-Specific Responses

Target TissueReceptorEffect of Epinephrine

-Heartβ₁↑ Heart rate (chronotropy), ↑ contractility (inotropy)

-Lungsβ₂Bronchodilation (opens airways)

-Blood Vesselsα₁Vasoconstriction (↑ BP) in skin & GI tract

-Blood Vesselsβ₂Vasodilation in skeletal muscle (↑ blood flow)

-Liverβ₂↑ Glycogenolysis → ↑ blood glucose

-Fat tissueβ₃↑ Lipolysis → energy release

-Pancreasα₂↓ Insulin secretion

Phenylephrine (Neo-Synephrine).

🔬 Mechanism of Action of Phenylephrine:

Phenylephrine is a selective α₁-adrenergic receptor agonist.

How It Works (Cellular Level):

-Binds to α₁-adrenergic receptors on vascular smooth muscle.

-Increased intracellular calcium causes smooth muscle contraction.

💉 Physiologic Effects:

-SystemEffectVascular systemVasoconstriction → ↑ SVR, ↑ BP

-CardiacMay cause reflex bradycardia via baroreceptors

⚠️ Does NOT:

Act on β₁ or β₂ receptors (so no direct cardiac stimulation or bronchodilation)

🏥 Common Uses in Clinical Settings:

-Hypotension (especially due to anesthesia)

-Off-label: to prolong spinal anesthesia or reduce bleeding in surgery

Dopamine

MOA: It is a catecholamine neurotransmitter and a hormone. . It is synthesized from the amino acid tyrosine, which is first converted to L-Dopa and then to dopamine by the enzyme DOPA decarboxylase.

These enzymes metabolize dopamine into homovanillic acid which is then excreted in the kidneys. Mostly B1 Agonist (inotropic, chronotropic, kidneys)

-low dose (1-2 mcg/kg/min)stimulates dopaminergic receptors, leading to vasodilation in renal, mesenteric, coronary, and cerebral vascular beds.

-Med Dose (2-10): Increase cardiac output and heart rate by stimulating beta-1 adrenergic receptors

-High doses (10-20) stimulates beta-1 adrenergic receptors, enhancing cardiac output, and at even a higher dose it activates alpha 1 adrenergic receptors causing vasoconstriction.

-Indications: Heart failure, shock, acute renal failure, improve cardio output and renal perfusion

Dosage: Low 2-5 mcg/kg/min to target dopaminergic and increased up to 20 mcg/kg/min for alpha and beta adrenergic effects such as tachycardia and arrhythmias.

Dobutamine

Mechanism of Action: Dobutamine

Dobutamine is a synthetic catecholamine and a β₁-adrenergic receptor agonist with mild β₂ and α₁ effects. It is primarily used for cardiac support in conditions like heart failure and cardiogenic shock.

🔬 Receptor Activity:

β₁ (dominant effect): Positive inotropy (↑ contractility) and mild to moderate chronotropy (↑ heart rate) ↑ Contractility, ↑ CO with minimal effect on HR or SVR

β₂ (mild): Vasodilation

α₁ (mild): Vasoconstriction (offsets β₂ effect slightly)

Cellular Mechanism:

-Dobutamine binds to β₁ receptors .

increased myocardial contractility (positive inotropic effect).

-Also increases AV conduction and HR (positive chronotropy)

Physiologic Effects:

EffectResult

-↑ Contractility↑ Cardiac Output (CO)

-↑ Heart Rate (moderate)↑ Cardiac Output

-Mild ↓ SVR (β₂ effect)↓ Afterload slightly

-Mild α₁ effectMinimal vasoconstriction.

Hemodynamic Summary:

↑ Cardiac Output

↑ Stroke Volume

↑ Myocardial O₂ demand

BP usually unchanged or slightly ↑ (due to balanced β₂ vasodilation and α₁ vasoconstriction)

Clinical Uses:

Cardiogenic shock

Acute heart failure

After cardiac surgery to improve contractility

Vasopressin

Vasopressin

MOA: Also known as antidiuretic hormone, It is released into the bloodstream in response to increases in plasma osmolality or decrease in blood volume.

V1: G-protein coupled receptor, leads to increased in intracellular calcium, causing vasoconstriction.

V2: located on renal tubes, stimulates increase in permeability of the renal ducts, resulting in fluid retention and increased preload.

Breakdown: it is broken down primarily in the liver and kidneys. Its half life is short, 10-20 min

Indication: Used when catecholamines are not working for septic shock. Dosage 0.04 units/min

A-Line

🩸 How an A-Line Works:

1.) Insertion:

Common sites: radial, femoral, brachial, or dorsalis pedis artery.

Inserted using sterile technique, often under ultrasound guidance.

2.) Fluid-Filled System:

The catheter is connected to:

Tubing filled with saline (non-compressible)

A pressure transducer

A monitor

The system is kept under continuous pressure (~300 mmHg) using a pressure bag to prevent blood backflow and maintain patency.

3.) Transducer Mechanics:

As the heart beats, it creates pulsatile arterial pressure.

This pressure is transmitted via the saline column to the transducer, which converts the pressure into an electrical signal.

The signal is displayed on a monitor as a waveform and a numerical reading.

🧠 Quick Tip for Nursing/ICU:

Always zero the transducer at the level of the phlebostatic axis (4th intercostal space, mid-axillary line) to ensure accurate readings.

🫀 1. Anacrotic Rise (Systolic Upstroke)

What it is: Sharp, steep rise on the left side of the waveform.

What it represents: Left ventricular contraction (systole) ejecting blood into the aorta.

Correlates with: The systolic blood pressure.

💓 2. Dicrotic Notch (Incisura)

What it is: A small downward deflection after the peak.

What it represents: Closure of the aortic valve.

Marks the transition from systole to diastole.

Very important for waveform interpretation — its absence or shift can suggest issues with timing or damping.

💧 3. Diastolic Runoff

What it is: Gradual downward slope after the dicrotic notch.

What it represents: Blood leaving the arteries into the peripheral circulation.

Correlates with: The diastolic blood pressure.

PAP

-Pulmonary artery pressure (aline for the R side of the heart

-Quarter/Dime (25/10)

Beta Blockers

Work by blocking the effects of adrenaline on the beta-adrenergic receptors of the heart and blood vessels. This action reduces heart rate, blood pressure, and 02 demand by the heart. Use with caution in Asthma pts due to potential respiratory effects

Atropine

Atropine is a muscarinic acetylcholine receptor antagonist. It works by blocking acetylcholine (ACh) from attaching to muscarinic receptors (M1-M5) found in various tissues. Blocks parasympathetic activity (anticholinergic effect). Specifically targets muscarinic receptors.

💓 Cardiac Effects (M2 receptors):

-Inhibits vagal stimulation on the SA node → ↑ heart rate

-Used to treat bradycardia

Respiratory Effects (M3 receptors):

-Bronchodilation

-Decreased bronchial secretions

Other Effects:

-Mydriasis (pupil dilation) and cycloplegia (loss of accommodation) by blocking M3 in the eye

-Decreased GI motility and urinary retention

⚠️ Clinical Uses:

-Bradycardia

-Pre-op to reduce secretions

-Antidote for organophosphate poisoning

-Pupil dilation for eye exams

What is a Beta Agonist?

usually used in respiratory conditions such as asthma and copd, as well as cardiac care. This drugs stimulate beta-adrenergic receptors, leading to muscular relaxation and bronchodilation, which is critical for relieving symptoms of bronchospasm.

Septic Shock

Systemic Shock happens everywheere

1.) Triggered by infection from any part of the body. The pathogens activates the body's immune response. Pathogens release molecules known as pathogen-associated molecular patters (PAMPs), which are detected by the body's Immune cells through pattern recognition receptors (PRRs) like Toll-like receptors.

2.) Activation of Innate Immunity: PAMPs are recognized by the innate immune cells (such as macrophages and neutrophils) are activated. These cells release a variety of signaling molecules including cytokines, chemokine, and other mediators. Cytokines like interleukin-1 (IL-1) and tumor necrosis factor-alpha play pivotal roles in mediating the inflammatory response. These cytokines not only help in fighting the infection but also signal other immune cells to join the response.

3.) Vascular changes and Systemic inflammation: The cytokines released during innate immune response induce vasodilation to increase blood flow to the affected area, facilitating the arrival of more immune cells. In sepsis this response is exaggerated and uncontrolled, leading to systemic vasodilation (Low SVR, Low BP, increased vascular permeability, and fluid leakage into tissues. This result is hypotension and reduced tissue perfusion (less red blood cells coming through), which are hallmark signs for sepsis.

Lower O2 to cells causes the body to go into Anaerobic metabolism which causes high lactate and acidosis

4.) Severe cases leads to cytokine storm, this refers to massive and uncontrolled release of cytokines into the bloodstream, which causes inflammation, tissue damage, and organ failure.

This can causes low SVR, DIC, ARDS

Septic Shock Hemodynamics and why?

Increased Cardiac output and HR

Decreased Systemic Vascular Resistance (800-1200 dynes/sec/cm5): vasodilation occurs in response to inflammatory mediators, leading to decreased resistance.

Decreased Pulmonary Capillary Wedge Pressure (PCWP): Reflects reduced blood volume and pressure in the cardiac system, often due to vasodilation and fluid shifting.

Cariogenic Shcok Hemodynamics

Decreased Cardiac Output: due to impaired cardiac function

Increased Systemic Vascular Resistance: As the body attempts to compensate for low cardiac output by constricting blood vessels.

Increased Pulmonary Capillary Wedge Pressure: Indicative of fluid congestion in the lungs due to heart failure

Hypovolemic Shock Hemodynamics

Decreased Cardiac output: result of low blood voume

Increased Systemic Vascular Resistance: increased as the body tries to maintain blood pressure by vasoconstriction.

Decreased Pulmonary Wedge Pressure: indicating reduced blood volume

Propofol

Propofol is a fast-acting, intravenous sedative-hypnotic agent. At the cellular level, it primarily acts on the central nervous system (CNS) by modulating ion channels—especially those linked to the inhibitory neurotransmitter GABA (gamma-aminobutyric acid). It is made up of soybean oil, Egg lecithin.

1. Targets GABA-A Receptors

-Propofol binds to and enhances the activity of GABA-A receptors.

-GABA- A = a ligand-gated chloride channel in the central nervous system (CNS).

-GABA (gamma-aminobutyric acid) is the brain's main inhibitory neurotransmitter.

2. Increases Chloride Influx

When GABA binds to its receptor, it opens the chloride channel.

Propofol enhances this effect → more Cl⁻ ions enter the neuron.

3. Hyperpolarization of Neurons

Increased chloride entry makes the inside of the neuron more negative.

This is called hyperpolarization.

A hyperpolarized neuron is less likely to fire an action potential (signal). This makes it harder for the neuron to fire(prevents excitation)

Continuous infusion:✅ 5–50 mcg/kg/min IV

S/S: vasodilation, lowers contractility

Anticonvulsant activity: Suppresses seizure activity through enhanced GABAergic tone

Rapid onset and recovery: High lipid solubility → fast CNS penetration & redistribution

GABA-A receptors are involved in:

Sedation and sleep

Anxiety control

Muscle relaxation

Seizure suppression

Blood flow through the heart

1-Superior & Inferior Vena Cava, Coronary Sinus

2-Rt Atrium,

3-Tricuspid Valve,

4- Rightt Ventricle,

5-Pulmonary Valve,

6-Pulmonary Artery, Right and Left

7- Lungs-pick up oxygen,

8-Pulmonary Veins, Left and Right

9- Left Atrium,

10- Mitral Valve (Bicuspid),

11-Left Ventricle,

12- Aortic Valve,

13-Aorta,

Brachio-cephalic trunk, Left common carotid artery, Left subclavian artery

14- Body

Precedex

Dexmedetomidine is a selective alpha-2 adrenergic receptor agonist, especially active in the central nervous system (CNS).

Dexmedetomidine binds to alpha-2 receptors in the locus coeruleus, a part of the brainstem that regulates arousal and wakefulness. By activating alpa 2 receptors (negative feedback) it prevents release of norepiphrine, which causes low HR and low BP

This activates Gi proteins (G-protein-coupled mechanism). Gi protein inhibits adenylate cyclase → ↓ cAMP.

Leads to inhibition of calcium channels and opening of potassium channels → hyperpolarization of neurons.

Result: Decreased neuronal firing, particularly in the sympathetic nervous system.

Activation of these receptors inhibits norepinephrine release, leading to:

-↓ Sympathetic nervous system activity

-↓ Alertness → sedation and anxiolysis

Stimulating alpha-2 receptors in vascular smooth muscle and the medulla leads to:

Decreased sympathetic tone

Bradycardia (slowed heart rate)

Hypotension (due to vasodilation)

Note: Initial bolus may cause transient hypertension due to peripheral alpha-2B stimulation

Dexmedetomidine acts like a "calm-down switch" in the brain and spinal cord. By reducing norepinephrine, it sedates, relaxes, and relieves pain—without knocking out breathing.

Alcohol withdrawal

🍺 Pathophysiology (What’s Going On in the Brain):

-Chronic alcohol use: Enhances GABA (inhibitory) activity and inhibits glutamate (excitatory).

Gaba is a chemical that is calming

Sudden cessation:

↓ GABA activity

Rebound ↑ glutamate and NMDA activity

Leads to CNS hyperexcitability → seizures, tremors, delirium

🚨 Delirium Tremens (DTs): ICU Emergency

Occurs in ~5% of patients with alcohol withdrawal

High mortality if untreated (~15–35%)

S/S:

Severe agitation and confusion, Anxiety, restlessness, tremors, hallucinations, seizures, delirium

Autonomic instability: ↑ HR, ↑ BP, fever

Hallucinations (esp. visual)

Diaphoresis, tremors

Possible cardiac arrhythmias,

💊 ICU Management:

Benzodiazepines (e.g. lorazepam, diazepam)First-line treatment to enhance GABA and prevent seizures/DTs

⚙️ Why Does Hypertension Occur in Alcohol Withdrawal?

1.) 🧠 Loss of CNS Inhibition

Chronic alcohol use enhances GABA (an inhibitory neurotransmitter) and suppresses glutamate (excitatory).

When alcohol is stopped:

GABA activity plummets

Glutamate activity rebounds (especially NMDA receptors)

Result: Excessive CNS excitability

2.) ⚡️ Autonomic Nervous System Overdrive

Increased sympathetic nervous system activity

This causes:

Vasoconstriction

Increased heart rate

Increased cardiac output

↑ Peripheral vascular resistance = ↑ Blood Pressure

3.) ⬆️ Catecholamine Surge

Elevated epinephrine and norepinephrine levels

These catecholamines:

Stimulate alpha-1 receptors → vasoconstriction → ↑ BP

Stimulate beta-1 receptors → ↑ HR and contractility

Ventilator Settings:

CMV

SIMV

PC

PS

PEEP

CMV (Controlled Mechanical Ventilation): Provides all the breathe for the patient, with no need for patient effort. Used when the pt is unable to initiate breaths adequately.

SIMV (Synchronized Intermittent Mandatory Ventilation):

Set tidal volume at the set breath rate, and all breaths above the set rate are spontaneous with the pt picking own tidal volume. Useful for weaning patients from mechanical. Lower set rate means the pt breaths more on their own.

PC (Pressure Control Ventilation): Delivers breaths at a set pressure, making it useful in protecting the lungs from high inflation pressures. This mode adjust the volume delivered based on the patient's lung compliance.

PSV (Pressure Support Ventilation):

Decreases work of breathing on the pt, pt receives an increase in airway pressure during inspiration to boost spontaneous tidal volume. Patient triggered mode. Helps to wean pt. All things are determined by the pt (Rate, Vt, Insp flow rate, Insp time.)

AC Mode (Assist-Control): Set tidal volume at the set breath rate, set tidal volume for each breath triggered by the pt spontaneously; Full vent support, can cause over ventilation

Plateau Pressure: Lung compliance, measured at end of insp want < 30

PEEP (Positive End-Expiratory Pressure): Positive pressure is applied to the airways at the end of exhalation. Increases lung volume, creating more surface area for gas exchange.

Ph 7.27

PaCo2 53

HCO3 23

Abd Ph

abd PaCo2

Normal HCo3

Uncompensated resp Acidosis

Ph 7.36

Paco2 49

HCO3 28

Normal PH

2 Abnormal Matching values

Fully Compensated Resp Acidosis

-lower ph is acidic so Co2 caused, body elevated bicarb to compensate

Ph 7.32

PaCo2 34

HCO3 20

Abnormal PH

matching Values

Comp but not complete

Metabolic Acidosis Partially Compensated

Fentanyl

Fentanyl is a potent synthetic opioid analgesic commonly used in anesthesia for pain control, blunting the stress response, and reducing anesthetic requirements. It is approximately 100 times more potent than morphine.

🔬 Cellular Mechanism of Action

Fentanyl acts primarily on mu-opioid receptors (μ-receptors) in the central nervous system (CNS) and spinal cord.

🧬 Step-by-step cellular action:

1.) Fentanyl binds to μ-opioid receptors

2.) Inhibits adenylyl cyclase → ↓ cAMP.

3.) Opens potassium (K⁺) channels → K⁺ efflux → hyperpolarization.

4.) Closes voltage-gated calcium (Ca²⁺) channels → ↓ neurotransmitter release (e.g., substance P, glutamate).

5.) → Inhibits pain transmission in the brain, brainstem, and spinal cord.

✅ Result: Profound analgesia, sedation, and blunted sympathetic response.

Respiratory depression: Dose-dependent ↓ respiratory drive (central apnea)

Bradycardia: Due to vagal stimulation

Chest wall rigidity:With rapid high-dose IV push; can impair ventilation

Nausea/vomiting:Common opioid side effect

Constipation:With repeated or chronic use

Hypotension:Rare, but possible with high doses (vasodilation)

🚨 Monitor closely for respiratory depression, especially when used with sedatives or other CNS depressants.

(can be titrated up to 10 mcg/kg/hr in some cases)

What type of shoe would you be?

Cowgirl boot: they are sturdy. dependable, and ready for anything. They are made for long days and all kinds of terrain. They are a symbol of grit and I know these are important qualities a CRNA needs in the OR.

Minute Ventilation

Tidal Volume x Respiratory Rate =

Normal is 4L/Min

Tidal Volume (VT) = 500 mL (0.5 L)

Respiratory Rate (RR) = 14 breaths/min

VE=0.5L×14=7L/min

👉 Minute ventilation = 7 L/min

News Occurring in the NA world today

AANA Hackathon first ever

Will you be among the Congress attendees tackling some of today's most urgent challenges in nurse anesthesiology?

Monday August 11 at 10am

Join nurse innovator and Hackathon host Rebecca Love, RN, MSN, FIEL, along with former AANA president and Beyond the Mask podcast host Sharon Pearce, DNP, CRNA, FAANA, FAAN, and 14 expert CRNA/nurse anesthesiologist mentors for an exclusive opportunity to collaborate, compete, and create real-world solutions.

How might CRNAs/nurse anesthesiologists lead innovations that improve perioperative brain health?

How might CRNAs/nurse anesthesiologists lead innovations that improve perioperative patient safety across diverse care settings?

How can AI be ethically and effectively integrated into anesthesia practice to support CRNA decision-making and improve patient safety?

Explain the Oxyhemoglobin-Dissociation Curve

Relates O2 saturation w/ blood PO2. And hemoglobins affinity for O2. How readily hemoglobin binds O2 in blood and releases in the tissues.

Left: Akalosis (Low H+), Low PaCo2, Hypothermia, Low 2, 3-DPG

Bad for tissues; SaO2 is high but O2 is stuck to Hgb

Right: Acidosis (High H+) , High PaCo2, Fever, High 2, 3-DPG, Good for tissues; SaO2 is low but O2 is easily released to the tissues.

R:right

I: Increased

G: DPG ^:

H: ^H+, Low ph (acidosis), High PaCo2

T: Temp ^

DPG attaches to red blood cells to help release O2 from Hb

ARDS

The body triggers an inflammatory response.

1.) Injury to the alveolar-capillary membrane triggers a massive release of proinflammatory cytokines. Type 1 alveolar cells are damaged during this time, their main goal is gas exchange

2.). Increased Capillary Permeability: The alveolar-capillary membrane becomes leaky Protein-rich fluid floods into the alveoli → causing non-cardiogenic pulmonary edema

🧫 3. Alveolar Collapse & Impaired Gas Exchange:

Type 2 Aveolar Cells are damaged. Surfactant production is reduced → increased surface tension causes alveoli lose stability and collapse (atelectasis)

Alveoli fill with fluid/debris → severe V/Q mismatch and shunting

PaO₂ drops despite high oxygen delivery

🏥 4. Decreased Lung Compliance & Stiff Lungs:

Fluid, inflammation, and collapse → lungs become stiff and non-compliant

Patient must work harder to breathe → may require mechanical ventilation

📉 5. Impaired Oxygenation (Hypoxemia):

Severe refractory hypoxemia (doesn’t improve with oxygen)

Defined as PaO₂/FiO₂ ratio < 300 (Berlin definition)

PaO2/ FIO2 ratio < 200 mmHG is ARDS

PAOP < 18 mm HG

ARDS Tx

🫁 Ventilator Settings for ARDS (Lung-Protective Strategy)

ARDS lungs are fragile. We aim to minimize ventilator-induced lung injury.

🔸 1. Low Tidal Volume (LTVV) (normal 6-8)

6 mL/kg of ideal body weight

Prevents overdistention (volutrauma), Permissive Hypercapnia

Accept higher PaCO₂ to protect lungs (as long as pH > 7.2)

Part of lung-protective strategy

-A low Vt will cause a rise in the PaCo2 and a drop in the pH

🔸 2. Plateau Pressure

Keep <30 cm H₂O

Monitors pressure in the alveoli during inspiration

Helps avoid barotrauma

🔸 3. PEEP (Positive End-Expiratory Pressure)

Usually moderate to high (≥5–15 cm H₂O)

Prevents alveolar collapse at end expiration (atelectasis)

Improves oxygenation and lung recruitment

🔸 4. FiO₂ (Fraction of Inspired Oxygen)

Start high (e.g., 100%) but titrate down to ≤60%

Goal: PaO₂ 55–80 mmHg or SpO₂ 88–95%

Reduce risk of oxygen toxicity

🔸 5. Respiratory Rate

Adjust to maintain adequate minute ventilation (to compensate for lower tidal volume)

Avoid respiratory alkalosis or permissive hypercapnia (if needed)

Others: Prone postiiton, No steroids

Usually the pt dies from MODS not hypoxemia

Cardiac Output

CO 4-8L/min

CO=HR x Stroke Volume (50-100 ml/beat)

HR and SV compensate for each other (HR high, SV low)

Contractility

-Squeeze your heart is able to do.

-Stroke Volume Index 35-60ml/beat/m2

-As contractility increases, the SV and CO increase

Pre-Load

-the volume/ pressure in the ventricle at the end of diastole after the AV values close. How much volume?

-CVP: R arterial pressure, R ventricle preload (2-8mmHG)

-PAOP (Pulm artery occlusion pressure): Left Atrium pressure (8-12mmHG)

-Frank Starling Law: more stretch more force

Stroke Volume formula

-Amount of blood ejected from the ventricle with each heartbeat

-50-100ml/beat

EDV (End Diastolic Volume) - ESV (End Systole Volume)

-EDV: Preload, volume in ventricle

-ESV: fluid remaining after contraction

Afterload

Resistance the heart must overcome to eject blood from the ventricle.

-As Afterload increases, SV and CO decrease

SVR (Systemic Vascular Resistance): measure of after load in the Left ventricle, 800-1200 dynes/s/cm-5

PVR (Pulmonary Vascular Resistance): measure of after load in the Right Ventricle, 100-250 dynes/s/cm-5