NSG 430 Exam 2: (Latest 2026/2027 Update) ADHF, AKI,
Cardiomyopathy, Dysrhythmias, & Pharmacology | Q&A | Grade A |
100% Correct (Verified Answers)
Subject: Advanced Medical-Surgical / Critical Care
Source: NSG 430 Exam 2 – Comprehensive Review Format: Q&A Guide with Clinical Rationale
1: What is acute decompensated heart failure (ADHF)?
Correct Answer: Exacerbation of chronic heart failure.
1. ADHF is a sudden or gradual worsening of HF symptoms requiring urgent therapy.
2. Often triggered by nonadherence, infection, ischemia, or dietary indiscretion.
3. Can lead to pulmonary edema if untreated.
2: What are the clinical manifestations of acute decompensated heart failure?
Correct Answer: Fluid overload, shortness of breath (SOB), fatigue.
1. Fluid overload results from reduced cardiac output and compensatory mechanisms.
2. SOB includes dyspnea, orthopnea, and paroxysmal nocturnal dyspnea.
3. Fatigue from decreased tissue perfusion and increased work of breathing.
3: What are the specific symptoms of acute decompensated heart failure?
Correct Answer: Jugular Vein Distension (JVD), edema, dyspnea, orthopnea, paroxysmal
nocturnal dyspnea, N/V, weight gain or loss, hepatomegaly, pulmonary rales, cardiac
gallops S3 or S4, pleural effusion.
1. JVD indicates elevated right atrial pressure (preload).
2. S3 gallop is hallmark of systolic HF; S4 suggests diastolic dysfunction.
3. Pulmonary rales indicate left ventricular failure with pulmonary congestion.
4: What can acute decompensated heart failure lead to?
Correct Answer: Pulmonary edema.
1. Pulmonary edema is a medical emergency with severe hypoxemia.
2. Results from acute elevation in left ventricular filling pressures.
3. Treatment includes O2, diuretics, and afterload reduction.
5: What is Acute Kidney Injury (AKI)?
Correct Answer: Abrupt reduction in renal function with elevated BUN, creatinine, and
Cystatin C levels (biomarker of kidney function). Usually associated with oliguria (<30 mL/hr
or <400 mL/day). GFR decreases. Can be reversed if diagnosed and treated early.
1. AKI develops over hours to days; early intervention improves outcomes.
2. Cystatin C is emerging biomarker not affected by muscle mass.
3. RIFLE classification: Risk, Injury, Failure, Loss, ESRD.
,6: What are the types of AKI?
Correct Answer: Prerenal, Intrarenal, Postrenal.
1. Prerenal: decreased renal blood flow (most common).
2. Intrarenal: direct damage to kidney parenchyma (ATN most common).
3. Postrenal: obstruction of urine outflow.
7: What labs are used to diagnose AKI?
Correct Answer: GFR, creatinine, electrolytes (particularly potassium).
1. Rising creatinine is the most reliable indicator despite lag time.
2. Hyperkalemia is a life-threatening complication of AKI.
3. BUN rises but is affected by hydration and protein intake.
8: What are symptoms of AKI?
Correct Answer: Fatigue, dizziness, swelling, decreased urine output, oliguria (<500 ml
urine), azotemia (increased urea in blood).
1. Oliguria is defined as <400 mL/day or <0.5 mL/kg/hr for 6 hours.
2. Azotemia reflects nitrogenous waste accumulation.
3. Fluid overload causes peripheral edema and pulmonary congestion.
9: What are interventions for AKI?
Correct Answer: Treat underlying cause of AKI, fluid restrictions, nutrition (enteral low
sodium/potassium/high calcium or TPN), medications (diuretics, calcium channel blockers -
drug of choice for AKI nephrotoxins), dose adjustment based on kidney function.
1. CCBs may protect against nephrotoxic injury by vasodilation.
2. Avoid nephrotoxic drugs: NSAIDs, aminoglycosides, contrast dye.
3. Fluid restriction: previous 24h losses + 600mL insensible losses.
10: What is Acute Tubular Necrosis (ATN)?
Correct Answer: Destruction of tubular epithelial cells with acute suppression of renal
function. Caused by poor blood flow/oxygenation to kidneys. Patients at risk: trauma,
massive transfusion. Nephrotoxic agents cause necrosis of tubular epithelial cells, which
slough off and plug tubules. Other risks: major surgery, shock, blood transfusion reaction,
muscle injury from trauma, prolonged hypotension.
1. ATN is the most common cause of intrarenal AKI.
2. Ischemic ATN: from prolonged prerenal state.
3. Nephrotoxic ATN: from contrast, aminoglycosides, myoglobin, hemoglobin.
11: What is Atenolol and its key effect?
Correct Answer: Bradycardia (slow heart rate less than 60 bpm).
1. Atenolol is a beta-blocker that reduces heart rate and contractility.
2. Used for hypertension, angina, and post-MI.
3. Monitor for hypotension and fatigue.
, 12: What are symptoms of bradycardia?
Correct Answer: Fatigue, low perfusion, shortness of breath, hypotension.
1. Symptomatic bradycardia requires treatment regardless of rate.
2. Low perfusion causes dizziness, syncope, altered mental status.
3. Hypotension may progress to cardiogenic shock.
13: What medication treats bradycardia?
Correct Answer: Atropine (increases heart rate).
1. Atropine blocks vagal tone to increase SA node rate.
2. Dose: 0.5 mg IV push, may repeat to 3 mg total.
3. If atropine ineffective, use transcutaneous pacing or dopamine/epinephrine.
14: What is another treatment for bradycardia if acute?
Correct Answer: Transcutaneous pacemaker.
1. TCP is temporary emergency pacing.
2. Provide analgesia/sedation due to discomfort.
3. Used until transvenous pacemaker or permanent pacemaker placed.
15: What are the types of cardiomyopathy?
Correct Answer: Dilated, hypertrophic, restrictive.
1. Dilated: enlarged ventricle, systolic dysfunction (most common).
2. Hypertrophic: thickened septum, diastolic dysfunction (young athletes).
3. Restrictive: stiff noncompliant ventricle (least common).
16: Describe dilated cardiomyopathy.
Correct Answer: Disease of heart muscle that causes heart to become enlarged and pump
less strongly. Mostly in elderly population.
1. Ejection fraction <40%; heart failure symptoms progressive.
2. Causes: ischemic heart disease, alcohol, viral, genetic.
3. Treatment: GDMT for HFrEF plus possible ICD/CRT.
17: Describe hypertrophic cardiomyopathy.
Correct Answer: Heart muscle becomes enlarged and blocks blood flow. Affects young
athletes.
1. Most common genetic heart disease; leading cause of sudden cardiac death in young athletes.
2. Dynamic left ventricular outflow tract obstruction.
3. Avoid dehydration, strenuous exercise, and drugs that reduce preload.
Cardiomyopathy, Dysrhythmias, & Pharmacology | Q&A | Grade A |
100% Correct (Verified Answers)
Subject: Advanced Medical-Surgical / Critical Care
Source: NSG 430 Exam 2 – Comprehensive Review Format: Q&A Guide with Clinical Rationale
1: What is acute decompensated heart failure (ADHF)?
Correct Answer: Exacerbation of chronic heart failure.
1. ADHF is a sudden or gradual worsening of HF symptoms requiring urgent therapy.
2. Often triggered by nonadherence, infection, ischemia, or dietary indiscretion.
3. Can lead to pulmonary edema if untreated.
2: What are the clinical manifestations of acute decompensated heart failure?
Correct Answer: Fluid overload, shortness of breath (SOB), fatigue.
1. Fluid overload results from reduced cardiac output and compensatory mechanisms.
2. SOB includes dyspnea, orthopnea, and paroxysmal nocturnal dyspnea.
3. Fatigue from decreased tissue perfusion and increased work of breathing.
3: What are the specific symptoms of acute decompensated heart failure?
Correct Answer: Jugular Vein Distension (JVD), edema, dyspnea, orthopnea, paroxysmal
nocturnal dyspnea, N/V, weight gain or loss, hepatomegaly, pulmonary rales, cardiac
gallops S3 or S4, pleural effusion.
1. JVD indicates elevated right atrial pressure (preload).
2. S3 gallop is hallmark of systolic HF; S4 suggests diastolic dysfunction.
3. Pulmonary rales indicate left ventricular failure with pulmonary congestion.
4: What can acute decompensated heart failure lead to?
Correct Answer: Pulmonary edema.
1. Pulmonary edema is a medical emergency with severe hypoxemia.
2. Results from acute elevation in left ventricular filling pressures.
3. Treatment includes O2, diuretics, and afterload reduction.
5: What is Acute Kidney Injury (AKI)?
Correct Answer: Abrupt reduction in renal function with elevated BUN, creatinine, and
Cystatin C levels (biomarker of kidney function). Usually associated with oliguria (<30 mL/hr
or <400 mL/day). GFR decreases. Can be reversed if diagnosed and treated early.
1. AKI develops over hours to days; early intervention improves outcomes.
2. Cystatin C is emerging biomarker not affected by muscle mass.
3. RIFLE classification: Risk, Injury, Failure, Loss, ESRD.
,6: What are the types of AKI?
Correct Answer: Prerenal, Intrarenal, Postrenal.
1. Prerenal: decreased renal blood flow (most common).
2. Intrarenal: direct damage to kidney parenchyma (ATN most common).
3. Postrenal: obstruction of urine outflow.
7: What labs are used to diagnose AKI?
Correct Answer: GFR, creatinine, electrolytes (particularly potassium).
1. Rising creatinine is the most reliable indicator despite lag time.
2. Hyperkalemia is a life-threatening complication of AKI.
3. BUN rises but is affected by hydration and protein intake.
8: What are symptoms of AKI?
Correct Answer: Fatigue, dizziness, swelling, decreased urine output, oliguria (<500 ml
urine), azotemia (increased urea in blood).
1. Oliguria is defined as <400 mL/day or <0.5 mL/kg/hr for 6 hours.
2. Azotemia reflects nitrogenous waste accumulation.
3. Fluid overload causes peripheral edema and pulmonary congestion.
9: What are interventions for AKI?
Correct Answer: Treat underlying cause of AKI, fluid restrictions, nutrition (enteral low
sodium/potassium/high calcium or TPN), medications (diuretics, calcium channel blockers -
drug of choice for AKI nephrotoxins), dose adjustment based on kidney function.
1. CCBs may protect against nephrotoxic injury by vasodilation.
2. Avoid nephrotoxic drugs: NSAIDs, aminoglycosides, contrast dye.
3. Fluid restriction: previous 24h losses + 600mL insensible losses.
10: What is Acute Tubular Necrosis (ATN)?
Correct Answer: Destruction of tubular epithelial cells with acute suppression of renal
function. Caused by poor blood flow/oxygenation to kidneys. Patients at risk: trauma,
massive transfusion. Nephrotoxic agents cause necrosis of tubular epithelial cells, which
slough off and plug tubules. Other risks: major surgery, shock, blood transfusion reaction,
muscle injury from trauma, prolonged hypotension.
1. ATN is the most common cause of intrarenal AKI.
2. Ischemic ATN: from prolonged prerenal state.
3. Nephrotoxic ATN: from contrast, aminoglycosides, myoglobin, hemoglobin.
11: What is Atenolol and its key effect?
Correct Answer: Bradycardia (slow heart rate less than 60 bpm).
1. Atenolol is a beta-blocker that reduces heart rate and contractility.
2. Used for hypertension, angina, and post-MI.
3. Monitor for hypotension and fatigue.
, 12: What are symptoms of bradycardia?
Correct Answer: Fatigue, low perfusion, shortness of breath, hypotension.
1. Symptomatic bradycardia requires treatment regardless of rate.
2. Low perfusion causes dizziness, syncope, altered mental status.
3. Hypotension may progress to cardiogenic shock.
13: What medication treats bradycardia?
Correct Answer: Atropine (increases heart rate).
1. Atropine blocks vagal tone to increase SA node rate.
2. Dose: 0.5 mg IV push, may repeat to 3 mg total.
3. If atropine ineffective, use transcutaneous pacing or dopamine/epinephrine.
14: What is another treatment for bradycardia if acute?
Correct Answer: Transcutaneous pacemaker.
1. TCP is temporary emergency pacing.
2. Provide analgesia/sedation due to discomfort.
3. Used until transvenous pacemaker or permanent pacemaker placed.
15: What are the types of cardiomyopathy?
Correct Answer: Dilated, hypertrophic, restrictive.
1. Dilated: enlarged ventricle, systolic dysfunction (most common).
2. Hypertrophic: thickened septum, diastolic dysfunction (young athletes).
3. Restrictive: stiff noncompliant ventricle (least common).
16: Describe dilated cardiomyopathy.
Correct Answer: Disease of heart muscle that causes heart to become enlarged and pump
less strongly. Mostly in elderly population.
1. Ejection fraction <40%; heart failure symptoms progressive.
2. Causes: ischemic heart disease, alcohol, viral, genetic.
3. Treatment: GDMT for HFrEF plus possible ICD/CRT.
17: Describe hypertrophic cardiomyopathy.
Correct Answer: Heart muscle becomes enlarged and blocks blood flow. Affects young
athletes.
1. Most common genetic heart disease; leading cause of sudden cardiac death in young athletes.
2. Dynamic left ventricular outflow tract obstruction.
3. Avoid dehydration, strenuous exercise, and drugs that reduce preload.
