ACS Recognition & Management
A patient presents with crushing left-sided chest pain radiating to the jaw, diaphoresis, and nausea. The pain does NOT improve with rest. What is the most likely diagnosis?
⭐ Bonus Question:
Why does radiation to the jaw/arm occur physiologically?
Most likely acute coronary syndrome (ACS), possibly an MI.
This presentation suggests myocardial ischemia due to reduced coronary blood flow. Pain that is non-reproducible and not relieved by rest is concerning for unstable angina or myocardial infarction rather than stable angina.
⭐ Bonus Answer:
Radiating pain occurs because visceral cardiac pain fibers share spinal pathways (T1–T5) with somatic nerves supplying the left arm, neck, and jaw — this is referred pain.
🧠 Exam trap: Pain reproducible with palpation suggests musculoskeletal cause.
A patient reports chest discomfort that occurs with exertion and resolves with rest. What type of angina is this, and what is happening physiologically?
⭐ Bonus Question:
Why does rest relieve the pain?
Stable angina.
This occurs when coronary arteries are narrowed by plaque. During exertion, oxygen demand increases, but narrowed arteries cannot supply enough blood → transient ischemia (no cell death).
⭐ Bonus Answer:
Rest reduces myocardial oxygen demand, allowing limited blood flow to meet needs again.
🧠 No troponin elevation in stable angina.
Why is aspirin given immediately in suspected ACS?
⭐ Bonus Question:
Why is it chewed instead of swallowed whole?
Aspirin inhibits platelet aggregation by blocking thromboxane A2 → prevents clot enlargement in coronary arteries.
⭐ Bonus Answer:
Chewing allows faster absorption through oral mucosa → quicker antiplatelet effect.
🧠 Time-sensitive clot prevention.
A patient presents with crackles, orthopnea, and pink frothy sputum. Which side of the heart is failing?
⭐ Bonus Question:
Why does this cause pulmonary symptoms?
Left-sided heart failure.
The left ventricle cannot pump effectively → blood backs up into pulmonary circulation → increased hydrostatic pressure → fluid leaks into alveoli.
⭐ Bonus Answer:
Fluid accumulation in alveoli impairs gas exchange, causing hypoxia and crackles.
🧠 Pink frothy sputum = pulmonary edema.
A patient with acute HF exacerbation is ordered IV furosemide. Why is IV preferred over oral in this setting?
⭐ Bonus Question:
What electrolyte must you monitor closely?
IV works faster and bypasses poor gut perfusion, which can occur in HF exacerbations. Rapid diuresis reduces preload and pulmonary congestion.
⭐ Bonus Answer:
Potassium. Loop diuretics cause potassium loss → risk for dysrhythmias.
🧠 Hypokalemia + digoxin = dangerous combo.
A patient’s troponin is elevated. What does this indicate?
⭐ Bonus Question:
Can troponin ever be elevated without an MI?
Elevated troponin indicates cardiac muscle injury.
Troponin is released when myocardial cells die. The higher the level and the longer it remains elevated, the more extensive the injury.
⭐ Bonus Answer:
Yes. Troponin can also rise in renal failure, severe heart failure, sepsis, or prolonged tachyarrhythmias — conditions that strain the heart.
🧠 Exam trap: Elevated troponin ≠ automatic STEMI. Look at EKG + clinical picture.
A patient’s lipid panel shows:
Total cholesterol 245
LDL 180
HDL 32
Triglycerides 210
Which values increase CAD risk?
⭐ Bonus Question:
Why is HDL protective?
All of those values increase CAD risk:
High total cholesterol
High LDL
Low HDL
High triglycerides
⭐ Bonus Answer:
HDL helps remove cholesterol from arteries (reverse cholesterol transport).
🧠 High LDL = plaque formation. Low HDL = less cleanup.
A patient with ACS receives sublingual nitro. After 5 minutes, pain persists and BP is 118/70. What do you do next?
⭐ Bonus Question:
What is the maximum number of SL doses typically given?
Administer a second dose (if BP stable).
⭐ Bonus Answer:
Up to 3 doses, 5 minutes apart.
🧠 Always reassess BP before each dose.
A patient with dyspnea has BNP 400 pg/mL. What does this suggest?
⭐ Bonus Question:
Why is BNP elevated in heart failure?
Elevated BNP suggests heart failure exacerbation.
⭐ Bonus Answer:
BNP is released from ventricles in response to stretching and volume overload.
🧠 BNP helps distinguish HF from pneumonia or COPD.
Why are ACE inhibitors used long-term in heart failure?
⭐ Bonus Question:
What lab value requires close monitoring?
They reduce afterload by blocking angiotensin II, lowering blood pressure and reducing cardiac workload. They also prevent ventricular remodeling.
⭐ Bonus Answer:
Potassium and creatinine. ACE inhibitors can cause hyperkalemia and worsen renal function.
🧠 Remodeling prevention improves survival.
An EKG shows ST elevation of ≥1 mm in two contiguous leads. What does this indicate?
⭐ Bonus Question:
What is the immediate goal in management?
This indicates a STEMI (ST-Elevation Myocardial Infarction) — a complete coronary artery occlusion.
The ST elevation reflects full-thickness (transmural) myocardial injury.
⭐ Bonus Answer:
Immediate reperfusion — get the patient to the cath lab for PCI (percutaneous coronary intervention).
🧠 Time is muscle. Delays increase myocardial death.
Why are statins prescribed for CAD even if cholesterol is only mildly elevated?
⭐ Bonus Question:
Beyond lowering LDL, what additional benefit do statins provide?
Statins reduce LDL and slow plaque progression.
⭐ Bonus Answer:
They stabilize plaque, reducing risk of rupture → lowers risk of ACS.
🧠 This is huge for preventing MI.
Why is morphine used cautiously in ACS?
⭐ Bonus Question:
What are two risks of morphine in MI patients?
Morphine reduces preload and anxiety, but can mask worsening symptoms and cause hypotension.
⭐ Bonus Answer:
Hypotension and respiratory depression; it may also delay absorption of oral antiplatelets.
🧠 Morphine is no longer “automatic.”
What is the difference between systolic and diastolic heart failure?
⭐ Bonus Question:
Which type typically has reduced ejection fraction?
Systolic HF = impaired contraction → reduced ejection fraction.
Diastolic HF = impaired relaxation/filling → preserved EF.
⭐ Bonus Answer:
Systolic HF has reduced EF (<40%).
🧠 HF with preserved EF still causes symptoms.
A patient on digoxin has nausea, confusion, and HR 52. What do you suspect?
⭐ Bonus Question:
What electrolyte abnormality increases digoxin toxicity risk?
Digoxin toxicity.
Bradycardia + GI symptoms + neuro changes are classic warning signs.
⭐ Bonus Answer:
Hypokalemia increases risk because digoxin competes with potassium at the Na⁺/K⁺ ATPase pump.
🧠 Always check apical pulse before giving.
You prepare to give sublingual nitroglycerin. BP is 92/58. What should you do?
⭐ Bonus Question:
Why can nitro cause reflex tachycardia?
Hold the nitroglycerin.
Nitro is a vasodilator. If BP is already low (<100 systolic is often used as a caution threshold), giving nitro can cause severe hypotension and reduce coronary perfusion.
⭐ Bonus Answer:
Vasodilation decreases blood pressure → body compensates with increased heart rate to maintain cardiac output.
🧠 Exam trap: Always check BP before nitro.
Why is a stress test useful in diagnosing stable CAD?
⭐ Bonus Question:
Why would a pharmacologic stress test be used instead of exercise?
Stress tests increase myocardial oxygen demand to reveal ischemia caused by narrowed arteries.
⭐ Bonus Answer:
Used when patients cannot physically exercise (mobility issues, deconditioning).
🧠 Stress-induced ST changes indicate ischemia.
Why are beta blockers given after MI?
⭐ Bonus Question:
When would you HOLD a beta blocker?
They reduce heart rate and myocardial oxygen demand, limiting infarct size and reducing arrhythmia risk.
⭐ Bonus Answer:
Bradycardia, hypotension, cardiogenic shock, acute decompensated HF.
🧠 Don’t give to a crashing patient.
A patient with HF suddenly develops severe dyspnea, BP 190/100, crackles, and O₂ sat 86%. What is happening?
⭐ Bonus Question:
What is your FIRST intervention?
Acute pulmonary edema.
⭐ Bonus Answer:
High Fowler’s position and oxygen immediately.
🧠 Oxygen before meds.
You have two HF patients:
Patient A: Weight gain 2 lbs overnight, mild ankle edema.
Patient B: New confusion, RR 32, crackles halfway up lung fields, O₂ 88%.
Who do you see first?
⭐ Bonus Question:
What complication is Patient B likely developing?
Patient B.
Signs suggest acute pulmonary edema and possible hypoxia.
⭐ Bonus Answer:
Acute decompensated heart failure with respiratory compromise.
🧠 ABCs always win.
A patient 24 hours after MI develops sudden shortness of breath and crackles bilaterally. What complication are you concerned about?
⭐ Bonus Question:
Why does this complication occur after MI?
Acute left-sided heart failure.
Damage to the left ventricle reduces pumping ability → blood backs up into pulmonary circulation → pulmonary edema → crackles and dyspnea.
⭐ Bonus Answer:
When the left ventricle cannot eject effectively, pressure increases in pulmonary veins → fluid leaks into alveoli.
🧠 This is why MI patients are monitored for HF signs post-event.
A patient with known CAD reports new chest pain that occurs at rest and lasts 20 minutes. Troponin is normal. EKG shows ST depression. What is this?
⭐ Bonus Question:
Why is this more dangerous than stable angina?
Unstable angina (part of ACS).
Plaque rupture has likely occurred with partial clot formation. Ischemia is occurring even without exertion.
⭐ Bonus Answer:
Unstable angina can quickly progress to MI because the plaque is unstable and thrombosis may worsen.
🧠 Exam trick: Normal troponin doesn’t mean “safe.”
When are thrombolytics used instead of PCI?
⭐ Bonus Question:
What is the most dangerous complication of thrombolytics?
When PCI is unavailable within appropriate time window and patient has STEMI.
⭐ Bonus Answer:
Hemorrhage, especially intracranial bleeding.
🧠 Always check bleeding history and BP.
A patient with chronic HF receives a 1L normal saline bolus in the ED. The next morning they are tachypneic with worsening crackles. Why did this happen?
⭐ Bonus Question:
Why must fluids be used cautiously in HF?
Volume overload worsened heart failure.
The failing ventricle cannot handle extra preload → pulmonary congestion.
⭐ Bonus Answer:
HF patients have limited cardiac reserve; excess fluids increase hydrostatic pressure and worsen edema.
🧠 This is a common exam trap.
A 72-year-old with CAD and HF presents with:
BP 86/52
HR 118
Crackles bilaterally
Cool, clammy skin
Decreased urine output
BNP elevated
What condition is developing?
⭐ Bonus Question:
Why is giving a fluid bolus dangerous here?
Cardiogenic shock.
The heart cannot pump effectively → poor perfusion + pulmonary congestion.
⭐ Bonus Answer:
The heart is failing as a pump; adding fluid increases preload and worsens pulmonary edema without improving cardiac output.
🧠 In cardiogenic shock, you support contractility (inotropes), not flood with fluids.