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CRNA: 1050 Online Flashcards

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CRNA (Certified Registered Nurse Anesthetist) exam prep: 1050 question-and-answer flashcards covering procedures, management, physiology. Try 30 free below — no sign-up required.

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📚 physiologymedium

A patient receives a 500 mL crystalloid bolus. How does this acutely alter the Left Ventricular (LV) pressure-volume loop?

#physiology#cardiology
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Card #1
Answer
Increased preload shifts the right side of the loop (End-Diastolic Volume, EDV) further to the right. This increases stroke volume (width of the loop) via the Frank-Starling mechanism. Rational: More filling = more stretch = more force. NBCRNA Note: Preload is the primary determinant of SV in the healthy heart. Distractor: It does not significantly change the End-Systolic Pressure-Volume Relationship (ESPVR) slope, which represents contractility.
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Card #1
2
📚 physiologymedium

Phenylephrine is administered to treat hypotension. What specific changes occur to the LV pressure-volume loop?

#physiology#cardiology
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Card #2
Answer
Phenylephrine increases SVR (afterload). The loop becomes taller and narrower. Specifically: 1) Increased End-Systolic Volume (ESV) - the loop's left boundary shifts right; 2) Increased peak systolic pressure; 3) Decreased Stroke Volume (SV). Clinical Pearl: High afterload opposes shortening, reducing SV unless contractility compensates. NBCRNA Tip: Watch for narrowing of the loop as a hallmark of increased afterload.
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Card #2
3
📚 physiologymedium

A patient is started on a Dobutamine infusion. How does the LV pressure-volume loop reflect this change in inotropic state?

#physiology#cardiology
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Card #3
Answer
Increased contractility increases the slope of the End-Systolic Pressure-Volume Relationship (ESPVR). The loop shifts to the left: 1) Decreased End-Systolic Volume (ESV); 2) Increased Stroke Volume (SV); 3) Increased Ejection Fraction (EF). Rationale: The ventricle empties more completely at any given afterload. Exam Strategy: ESPVR is the gold standard for assessing load-independent contractility on the PV loop.
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Card #3
4
📚 physiologymedium

During which phase of the cardiac cycle does the LV pressure fall most rapidly while the volume remains constant, and which valves are closed?

#physiology#cardiology
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Card #4
Answer
Phase: Isovolumetric Relaxation. Valves: Both Aortic and Mitral valves are closed. This begins after the aortic valve closes (dicrotic notch on arterial line) and ends when LV pressure falls below left atrial pressure, opening the mitral valve. NBCRNA Focus: This is an energy-consuming process (Lusitropy). Impairment (e.g., ischemia) leads to diastolic dysfunction.
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Card #4
5
📚 physiologymedium

On a standard LV pressure-volume loop, how is Stroke Volume (SV) graphically represented, and what is the formula using loop parameters?

#physiology#cardiology
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Card #5
Answer
SV is the horizontal width of the loop. Formula: SV = EDV - ESV (End-Diastolic Volume minus End-Systolic Volume). Clinical Significance: The area inside the loop represents Stroke Work (SW), which correlates with myocardial oxygen consumption (MVO2). Exam Tip: If the loop widens, SV has increased; if it narrows, SV has decreased.
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Card #5
6
📚 physiologyhard

A patient with severe Aortic Stenosis (AS) undergoes induction. What characteristic changes are seen on their LV pressure-volume loop compared to a normal loop?

#physiology#cardiology
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Card #6
Answer
1) Significantly higher peak LV systolic pressure (taller loop) to overcome the valvular gradient. 2) Narrower loop (decreased SV) due to high afterload. 3) Increased LV End-Diastolic Pressure (LVEDP) due to concentric hypertrophy and reduced compliance. Clinical Pearl: AS is a pressure overload state. NBCRNA emphasizes the need for full, slow, and constricted (maintain preload/SVR, avoid tachycardia).
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Card #6
7
📚 physiologyhard

Describe the LV pressure-volume loop changes in chronic Mitral Regurgitation (MR).

#physiology#cardiology
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Card #7
Answer
1) Absence of true isovolumetric phases (contraction and relaxation) because blood leaks into the LA as soon as the LV starts contracting. 2) Increased EDV (preload) due to the regurgitant volume returning from the LA. 3) Decreased ESV (LV empties into low-pressure LA). 4) Loop looks rounded or egg-shaped. Exam Strategy: MR is the classic volume overload state. NBCRNA Distractor: MR often shows a normal EF despite LV dysfunction because of the low-resistance exit into the LA.
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Card #7
8
📚 physiologyhard

How does the area within the LV pressure-volume loop relate to myocardial oxygen consumption (MVO2) and Stroke Work?

#physiology#cardiology
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Card #8
Answer
The area inside the loop equals Stroke Work (SW). MVO2 is determined by the Pressure-Volume Area (PVA), which is the sum of SW and the Potential Energy (PE) stored in the wall. Clinical Insight: Conditions increasing the area (e.g., high afterload or high SV) increase MVO2. Tachycardia and increased wall tension (Laplace) are the most significant drivers of MVO2 in the clinical setting.
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Card #8
9
📚 physiologyhard

An elderly patient with HFpEF shows a steeper End-Diastolic Pressure-Volume Relationship (EDPVR). What does this signify?

#physiology#cardiology
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Card #9
Answer
A steeper EDPVR signifies decreased LV compliance (increased stiffness). For any given volume (preload), the pressure (LVEDP) will be higher. This is the hallmark of diastolic dysfunction. Clinical Pearl: These patients are highly sensitive to small changes in volume; they develop pulmonary edema quickly with fluid boluses. NBCRNA Tip: Differentiate compliance (change in volume/pressure) from contractility (ESPVR).
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Card #9
10
📚 physiologyhard

In Aortic Regurgitation (AR), what specific changes occur to the phases of the LV pressure-volume loop?

#physiology#cardiology
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Card #10
Answer
1) No true isovolumetric relaxation: The LV fills from the aorta immediately after the aortic valve closes. 2) Massive increase in EDV (rightward shift). 3) Increased SV (widened loop) to compensate for backward flow. 4) High systolic pressure with low diastolic pressure (wide pulse pressure). Exam Strategy: AR is a combined pressure and volume overload state leading to eccentric hypertrophy.
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Card #10
11
📚 physiologymedium

Calculate the Coronary Perfusion Pressure (CPP) for a patient with a BP of 110/70 mmHg, a CVP of 10 mmHg, and a PAOP of 18 mmHg. Which value is the most critical determinant of LV perfusion?

#cardiology#hemodynamics
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Card #11
Answer
CPP = Diastolic Blood Pressure (DBP) - Left Ventricular End-Diastolic Pressure (LVEDP). Using PAOP as a proxy for LVEDP: 70 - 18 = 52 mmHg. Rationale: LV perfusion occurs almost exclusively during diastole. While MAP is used for other organs, DBP is the driving force for the coronaries. Aim for CPP >50-60 mmHg to prevent ischemia. Exam Strategy: NBCRNA often provides CVP as a distractor; remember that for the LV, LVEDP (or PAOP) is the specific downstream pressure, not CVP (which is the downstream pressure for the RV).
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Card #11
12
📚 physiologyhard

In a patient with severe pulmonary hypertension and RV hypertrophy, how does the timing of right coronary artery (RCA) blood flow change compared to a healthy patient?

#cardiology#pathophysiology
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Card #12
Answer
In a healthy heart, the RV is perfused during both systole and diastole because RV systolic pressure is lower than aortic diastolic pressure. In severe Pulmonary Hypertension (PH), RV systolic pressure may equal or exceed systemic pressure. Mechanism: This shifts RCA perfusion to be primarily diastolic (similar to the LV pattern). This makes the RV highly susceptible to ischemia if DBP drops or HR increases. Exam Tip: NBCRNA focuses on the LV-like behavior of the stressed RV. Maintain a high SBP/DBP in these patients to ensure a favorable pressure gradient (Aorta > RV pressure).
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Card #12
13
📚 physiologymedium

Rank the following factors in order of their impact on Myocardial Oxygen Demand (MVO2) from greatest to least: Heart Rate, Afterload, Contractility, Preload.

#cardiology#physiology
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Card #13
Answer
1. Heart Rate (Most significant) 2. Afterload (Wall Tension) 3. Contractility 4. Preload (Least significant) Rationale: Tachycardia is the most detrimental because it increases demand while simultaneously decreasing supply (shorter diastolic time). Preload (volume work) is relatively cheap in terms of O2 consumption compared to pressure work (afterload). Clinical Pearl: This is why beta-blockers are cardioprotective—they target the most oxygen-expensive variable (HR).
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Card #13
14
📚 physiologyhard

Which metabolic byproduct is considered the primary mediator of coronary vasodilation during periods of increased myocardial oxygen demand, and what is its mechanism?

#cardiology#pharmacology
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Card #14
Answer
Adenosine. Mechanism: When O2 demand exceeds supply, ATP breakdown increases, leading to adenosine accumulation. Adenosine binds to A2 receptors on vascular smooth muscle, increasing cAMP and causing vasodilation. Other mediators: Nitric Oxide (shear stress), CO2, H+, and K+ channels. Exam Strategy: Differentiate between Autoregulation (MAP 60-140 mmHg) and Metabolic Regulation. If MAP is within range, flow is constant; if demand increases, metabolic regulation overrides to increase flow.
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Card #14
15
📚 physiologymedium

What is the typical myocardial oxygen extraction ratio (ERO2), and how does the heart primarily compensate for increased oxygen demand?

#cardiology#physiology
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Card #15
Answer
The heart extracts 70–80% of delivered oxygen at rest (compared to 25% for the whole body). Compensation: Because the extraction is already near maximal, the heart has no extraction reserve. Therefore, any increase in demand MUST be met by a nearly linear increase in Coronary Blood Flow (CBF). Clinical Significance: This makes the heart uniquely vulnerable to fixed stenoses (CAD) where flow cannot increase to meet demand, leading to immediate ischemia.
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Card #15
16
📚 physiologyhard

Describe the mechanism of Anesthetic-Induced Preconditioning (APC) provided by volatile agents like Sevoflurane.

#pharmacology#cardiology
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Card #16
Answer
Mechanism: Volatile anesthetics trigger a signaling cascade (involving G-proteins and Protein Kinase C) that culminates in the opening of mitochondrial ATP-sensitive potassium (mKATP) channels. Effect: This mimics the body's natural ischemic preconditioning, protecting the myocardium against reperfusion injury and reducing infarct size. Exam Strategy: NBCRNA tests the cardioprotective benefits of volatiles. Note that Nitrous Oxide and certain IV agents (like Ketamine) may lack these benefits or potentially interfere with them.
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Card #16
17
📚 physiologymedium

Using the Law of LaPlace, explain why ventricular hypertrophy is a compensatory mechanism for chronic hypertension, and identify the cost to MVO2.

#cardiology#physics
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Card #17
Answer
Law of LaPlace: Wall Tension = (Pressure x Radius) / (2 x Wall Thickness). Rationale: By increasing wall thickness (hypertrophy), the ventricle reduces the wall tension required to generate the high pressures needed to overcome systemic afterload. The Cost: While it reduces tension per unit of muscle, the increased muscle mass (hypertrophy) increases total MVO2 and can compress subendocardial vessels, worsening the supply-demand balance. Exam Tip: Recognize that Concentric Hypertrophy (pressure overload) is more O2-expensive than Eccentric Hypertrophy (volume overload).
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Card #17
18
📚 physiologyhard

Explain the phenomenon of Coronary Steal and identify which pharmacological agent is most traditionally associated with it in the clinical setting.

#cardiology#pharmacology
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Card #18
Answer
Coronary Steal occurs when a potent vasodilator (e.g., Adenosine, Dipyridamole) dilates healthy coronary vessels, stealing blood flow away from collateral-dependent ischemic areas that are already maximally dilated. Clinical Context: While Isoflurane was historically debated, it is rarely clinically significant at standard MAC. Pharmacological stress testing (Adenosine) is the classic example. Exam Strategy: Focus on the concept that blood follows the path of least resistance. In the presence of a steal prone anatomy (multivessel disease), global vasodilation can worsen regional ischemia.
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Card #18
19
📚 physiologymedium

Which three factors determine Myocardial Oxygen Supply? Identify the factor most easily manipulated by the CRNA during the maintenance phase of anesthesia.

#cardiology#physiology
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Card #19
Answer
1. Coronary Blood Flow (CBF = CPP / Coronary Vascular Resistance) 2. Arterial Oxygen Content (CaO2) 3. Diastolic Time (Heart Rate) CRNA Manipulation: Heart Rate is the most easily manipulated variable. By maintaining a slow, steady HR, the CRNA maximizes diastolic time (supply) and minimizes MVO2 (demand). Formula Check: CaO2 = (Hgb x 1.34 x SaO2) + (PaO2 x 0.003). While Hgb is important, acutely controlling HR is the primary intraoperative maneuver for supply-demand balance.
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Card #19
20
📚 physiologyhard

Why is the subendocardium the most vulnerable layer of the heart to ischemia, especially during tachycardia or hypotension?

#cardiology#pathophysiology
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Card #20
Answer
1. High Tissue Pressure: Subendocardial vessels are compressed by high LV intracavitary pressures during systole. 2. Perfusion Timing: Perfusion occurs only in diastole. 3. Metabolic Demand: The subendocardium has the highest O2 demand due to higher wall tension (LaPlace). Clinical Indicators: ST-segment depression in Lead II or V5 often reflects subendocardial ischemia. Exam Strategy: When CPP (DBP - LVEDP) falls, the subendocardium is the first to suffer. NBCRNA often asks about the Supply/Demand ratio (DPTI/SPTI), where a ratio <0.4 indicates high risk for subendocardial ischemia.
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Card #20
21
📚 pathologymedium

A 75yo male with severe aortic stenosis (AVA 0.8 cm²) is scheduled for TAVR. What are the specific hemodynamic goals for heart rate and rhythm, and why?

#pathology#cardiology
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Card #21
Answer
Goals: Slow, Sinus, Full. HR 60-80 bpm. Sinus rhythm is critical as the atrial kick contributes up to 40% of LVEDV in a non-compliant, hypertrophied LV. Avoid tachycardia (increases O2 demand, decreases supply time) and bradycardia (decreases CO due to fixed stroke volume). Maintain high-normal preload to overcome decreased LV compliance. Maintain SVR to ensure coronary perfusion pressure. NBCRNA Tip: AS is a pressure-overload lesion leading to concentric hypertrophy.
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Card #21
22
📚 pathologymedium

A pregnant patient with mitral stenosis (MS) presents for urgent C-section. Which hemodynamic change during labor is MOST likely to cause acute pulmonary edema?

#pathology#cardiology
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Card #22
Answer
Tachycardia. MS is a flow-restricted lesion; the stenotic valve limits LV filling. Increased HR shortens diastolic filling time, causing a backup of pressure into the left atrium and pulmonary vasculature. Hemodynamic goals: Slow, Sinus, Dry. Maintain a slow HR (50-70 bpm) and avoid fluid boluses that increase LAP. Exam Strategy: Pain/stress-induced tachycardia is the primary trigger for decompensation in MS patients. Beta-blockade is the LATEST first-line treatment for rate control.
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Card #22
23
📚 pathologymedium

A patient with chronic aortic regurgitation (AR) is undergoing non-cardiac surgery. What is the rationale for maintaining a Fast, Forward, Full hemodynamic profile?

#pathology#cardiology
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Card #23
Answer
Fast (HR 80-100) shortens diastole, reducing the time for regurgitant flow back into the LV. Forward (decreased SVR/afterload) promotes systemic flow over retrograde flow. Full (adequate preload) maintains SV in an eccentrically dilated LV. High-yield: Acute AR (e.g., endocarditis) is a surgical emergency because the LV hasn't had time to adapt/dilate, leading to rapid-onset pulmonary edema and cardiogenic shock.
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Card #23
24
📚 pathologymedium

During anesthetic induction for a patient with severe mitral regurgitation (MR), which physiological change will most likely INCREASE the regurgitant fraction?

#pathology#cardiology
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Card #24
Answer
Increased Afterload (SVR). MR is highly sensitive to the pressure gradient between the LV and LA. Increased SVR or bradycardia (prolonged systole) increases the volume of blood pushed back into the LA. Hemodynamic goals: Fast, Forward, Full. Vasodilation (decreased SVR) is beneficial. Avoid factors that increase PVR if secondary pulmonary HTN is present. NBCRNA Focus: Distinguish MR (eccentric hypertrophy) from MS (LA enlargement/AFib risk).
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Card #24
25
📚 pathologyhard

On a Pressure-Volume (PV) loop, how does severe aortic stenosis typically alter the appearance of the loop compared to a normal heart?

#pathology#cardiology
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Card #25
Answer
The loop shifts Up and Right. Key features: 1) Narrower loop (decreased stroke volume). 2) Significantly higher peak systolic pressure (increased LV pressure required to overcome the stenotic valve). 3) Increased LVEDP (due to decreased compliance/concentric hypertrophy). The area within the loop (Stroke Work) increases significantly, explaining the very high myocardial oxygen demand and risk for subendocardial ischemia even without CAD.
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Card #25
26
📚 pathologymedium

According to current 2026 AHA/ACC guidelines, what specific echocardiographic findings define Stage D (Symptomatic Severe) Aortic Stenosis?

#pathology#cardiology
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Card #26
Answer
1) Aortic Valve Area (AVA) ≤ 1.0 cm². 2) Mean Gradient ≥ 40 mmHg. 3) Peak Velocity ≥ 4.0 m/s. Exam Tip: Be aware of Low-flow, low-gradient AS where EF is reduced (<50%), but the valve is still severe (AVA < 1.0); this often requires dobutamine stress echocardiography to differentiate from pseudo-stenosis where the valve doesn't open simply because the pump is weak.
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Card #26
27
📚 pathologyhard

A patient presents with acute aortic regurgitation (AR) due to infective endocarditis. Why is the use of an Intra-Aortic Balloon Pump (IABP) absolutely contraindicated in this scenario?

#pathology#cardiology
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Card #27
Answer
IABP inflation occurs during diastole, which would significantly increase the volume of blood regurgitating through the incompetent aortic valve into the LV. This causes catastrophic LV distension, increased LVEDP, and acute heart failure. Management: Rapid surgical intervention and afterload reduction (e.g., Nitroprusside) if BP allows. Avoid beta-blockers in acute AR as they block the compensatory tachycardia needed to maintain cardiac output.
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Card #27
28
📚 pathologyhard

A patient with Hypertrophic Obstructive Cardiomyopathy (HOCM) develops Systolic Anterior Motion (SAM) of the mitral valve. What is the primary anesthetic management priority?

#pathology#cardiology
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Card #28
Answer
Increase Preload and Afterload; Decrease Contractility. SAM occurs when the anterior mitral leaflet is sucked into the LVOT during systole, causing obstruction and secondary MR. Treatment: Esmolol (decrease HR/contractility), Phenylephrine (increase SVR to splint the LVOT open), and IV fluids. Distractor: Do NOT use Inotropes (Dobutamine) or Vasodilators (Nitroglycerin), as they worsen the LVOT gradient by making the heart empty and hyperdynamic.
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Card #28
29
📚 pathologyhard

Explain the mathematical relationship between heart rate and the pressure gradient across a stenotic mitral valve as it relates to pulmonary congestion.

#pathology#cardiology
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Card #29
Answer
The pressure gradient is proportional to the square of the flow rate (Gorlin Equation). As HR increases, diastole (filling time) shortens. To maintain stroke volume, the flow rate across the valve must increase during that shorter window. This exponentially increases the LA-LV pressure gradient, leading to rapid increases in LA pressure and pulmonary venous congestion. This is why beta-blockade and HR control are the cornerstones of MS management.
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Card #29
30
📚 pathologyhard

In a patient with severe Tricuspid Regurgitation (TR) and secondary Right Ventricular (RV) failure, what is the most critical ventilator parameter to manage?

#pathology#cardiology
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Card #30
Answer
Peak Inspiratory Pressure (PIP) and PEEP. High airway pressures increase Pulmonary Vascular Resistance (PVR), which increases RV afterload and worsens TR. Management: Maintain low PIP, avoid hypoxia/hypercarbia/acidosis (all increase PVR), and maintain Full RV preload (high-normal CVP) while avoiding over-distension. NBCRNA Tip: TR is often secondary to left-sided failure; always look for the primary cause (e.g., Mitral Stenosis).
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Card #30

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About This Collection

I have spent years guiding nurses through the rigorous transition to anesthesia practice, and if there is one thing I emphasize to every candidate, it is that shallow review simply does not cut it. The board exam is not merely about memorizing facts; it is about synthesizing complex information under pressure to make life-saving decisions. To truly succeed, you need a systematic approach that covers every angle of the curriculum with precision and depth. In this complete collection of 1,050 flashcards, the focus is on total content mastery rather than quick recall. When I review the physiology and pathology sections with my mentees, we dig into the mechanisms of action, not just the outcomes. We cover pharmacodynamics and pharmacology in detail because understanding the specific interactions of anesthetics is just as critical as knowing the standard dosages. This level of comprehensive coverage is necessary to handle the nuance found in modern board questions, where multiple answers often seem correct. I often tell my colleagues that passing the exam is just the first step; being a safe, competent provider is the ultimate goal. The content here, spanning equipment, diagnostics, and electrical safety, helps bridge that gap. I have seen too many students struggle because they could not visualize the clinical application of a concept during the exam. By integrating management strategies, assessment protocols, and procedural steps into your daily study routine, you are not just prepping for a test, you are mentally rehearsing for the reality of the operating room. Through my experience mentoring hundreds of successful candidates, I have found that consistency beats intensity every time. Trying to cram thousands of pages of text is a recipe for burnout. Instead, using these 1,050 cards allows for active recall and spaced repetition, methods I always recommend for long-term retention. Whether you are reviewing assessment techniques or revisiting the basics of anesthesia equipment, doing a specific number of cards every day builds a foundation that does not crumble under exam stress. This collection represents a significant commitment to your education and your future practice. It takes discipline to work through over a thousand complex concepts, but the confidence you gain is worth the effort. I encourage you to approach this material with curiosity and diligence. You are building the knowledge base that will support your clinical judgment for the rest of your career.