Module 7 — Cardiac Guided Notes

Baseline first. You cannot call something abnormal until you know what normal looks like.

Normal Findings

• Normal heart rate: 60 to 100 bpm
• Normal rhythm: normal sinus rhythm — regular R–R intervals, one upright P wave before every QRS
• Normal capillary refill: Less than 3 seconds (many texts use <2 seconds — either way it should be brisk; sluggish refill = poor peripheral perfusion)
• Skin should be: warm, dry, intact, and normal color for the patient — no pallor, cyanosis, mottling, or diaphoresis
• Peripheral pulses should be: palpable, regular, equal bilaterally, and 2+ (normal) in strength

Pulse scale: 0 = absent · 1+ = weak/thready · 2+ = normal · 3+ = full · 4+ = bounding.

Think Like a Nurse 🧠

Which finding concerns you more?

• HR 55 while sleeping — ❌ Expected. Vagal tone rises during sleep; an asymptomatic, perfusing patient with HR 55 is not the emergency.
• HR 110 with chest pain and diaphoresis — ✅ This one. Tachycardia + chest pain + diaphoresis is the classic ACS picture.

Why? A number alone is never the answer — symptoms are. HR 55 in a comfortable sleeping patient is a normal variant, but HR 110 with chest pain and diaphoresis means the heart is ischemic and the sympathetic system is compensating. Faster rate also shortens diastole, which is exactly when the coronary arteries fill, so ischemia feeds itself.

🤖 Ask Claire: "Explain normal versus abnormal cardiac assessment findings and quiz me with 3 questions."

Fill in the Blanks

• CAD occurs when atherosclerotic plaque (fatty/cholesterol deposits, mostly LDL, plus inflammatory cells and fibrous tissue) builds up inside the coronary arteries.
• This reduces blood flow → oxygen delivery (myocardial perfusion) to the heart muscle.

Common Risk Factors

Modifiable: hypertension, hyperlipidemia (↑ LDL, ↓ HDL), smoking/vaping, diabetes mellitus, obesity (especially central), physical inactivity, high-sodium and high-saturated-fat diet, chronic stress, excess alcohol

Non-modifiable: age (men >45, women >55), male sex or postmenopausal female, family history of premature CAD, genetics/ethnicity

Diabetes is the sneaky one — because neuropathy blunts pain, diabetics can infarct without ever reporting chest pain.

Memory Tip

Blocked artery = less oxygen = chest pain.

Think Like a Nurse 🧠

A patient develops chest pain while climbing stairs but feels better after resting. Why did the pain stop?

Resting dropped myocardial oxygen demand back below what the narrowed artery can supply. The plaque is still there — the pain stopped because demand fell, not because the blockage cleared. That supply/demand pattern is the definition of stable angina.

🤖 Ask Claire: "Give me one patient scenario with CAD and make me identify the pathophysiology."

Stable Angina

• Occurs with: exertion or anything that raises oxygen demand — exercise, stairs, emotional stress, heavy meals, cold air. Predictable and reproducible; usually lasts <5–15 minutes
• Improves with: rest (within a few minutes)
• May improve after taking: sublingual nitroglycerin 0.4 mg — relief usually within 5 minutes

Unstable Angina

• Occurs: at rest, with minimal exertion, or as new-onset pain — and is increasing in frequency, severity, or duration. Unpredictable, and NOT relieved by rest or nitroglycerin
• Is considered a warning sign for: myocardial infarction — it is part of acute coronary syndrome and means a plaque has ruptured with partial clot formation

💊 Nitroglycerin rules you must know

Quick Check

Nitroglycerin no longer relieves the patient's chest pain. What should you suspect?

Acute coronary syndrome — assume myocardial infarction until proven otherwise. Unrelieved pain means the vessel is occluded, not just narrowed. Priority: stay with the patient, get a 12-lead ECG within 10 minutes, notify the provider/activate the chest-pain protocol, give aspirin, and draw troponin.

Remember

Stable = predictable. Unstable = dangerous.

ACS is an umbrella term for sudden, reduced blood flow to the heart. Select all that apply:

• Stable angina — ❌ NOT included. It is chronic, predictable CAD, not an acute plaque event.
• Unstable angina — ✅ Included. Ischemia at rest with a negative troponin.
• NSTEMI — ✅ Included. Partial occlusion with a POSITIVE troponin (myocardial cells died).
• STEMI — ✅ Included. Complete occlusion, ST elevation, positive troponin — the most urgent.

One-line separator: UA vs NSTEMI = troponin. NSTEMI vs STEMI = ST elevation.

Common Symptoms

Classic: substernal chest pressure/tightness/heaviness radiating to the left arm, jaw, neck, shoulder, or back; unrelieved by rest or nitro; lasting >15–20 minutes

Plus: dyspnea, diaphoresis (cold clammy sweat), nausea/vomiting, dizziness, extreme fatigue, palpitations, anxiety or a sense of impending doom, pallor, tachycardia

Atypical (women, older adults, diabetics): shortness of breath, unusual fatigue or weakness, indigestion/epigastric pain, back or jaw pain, nausea, syncope — often with NO chest pain at all ("silent MI")

Think Like a Nurse 🧠

A diabetic patient reports nausea and sweating but no chest pain. Should ACS still be considered?

• Yes — ✅ Correct.
• No — ❌ Wrong — this is exactly the patient who dies from a missed MI.

Why? Diabetic autonomic neuropathy blunts the pain signal, so a diabetic can infarct silently. Nausea and diaphoresis are sympathetic/vagal responses to ischemia and count as anginal equivalents. Treat this as ACS until ruled out: 12-lead ECG within 10 minutes, troponin, continuous monitoring, aspirin.

🤖 Ask Claire: "Create 3 ATI-style ACS questions that require me to identify the most concerning assessment finding."

Fill in the Blanks

An MI occurs when blood flow to the heart is blocked long enough to cause: irreversible myocardial cell death (necrosis/infarction). Ischemia is reversible; infarction is not — and necrosis begins within about 20–30 minutes of complete occlusion, which is why time = muscle.

Priority Assessments

• Monitor ECG because: lethal dysrhythmias are the #1 cause of death in the first hours after an MI — ventricular fibrillation especially. The ECG also shows whether the infarct is extending (new/worsening ST changes).
• Monitor urine output because: urine output is a direct window into perfusion. Less than 30 mL/hr means the kidneys are not being perfused, which means cardiac output has fallen — an early sign of cardiogenic shock.
• Monitor BP because: a falling BP means the pump is failing (cardiogenic shock), and adequate systolic pressure is also required before giving nitroglycerin, morphine, or beta blockers. Coronary arteries perfuse during diastole — hypotension worsens the infarct.

💊 MONA — then vs. now

She still teaches the mnemonic, but the modern evidence changed how it's used. Know both.

Also standard now: P2Y12 inhibitor (clopidogrel/ticagrelor), anticoagulant (heparin), high-intensity statin, beta blocker within 24 h if not in shock, ACE inhibitor.

Think Like a Nurse 🧠

Your patient is pale, diaphoretic, BP 82/48, HR 120, and increasingly restless. What complication worries you most?

Cardiogenic shock. The infarcted muscle can no longer pump, so cardiac output falls → hypotension, compensatory tachycardia, cold clammy vasoconstricted skin. Restlessness is early cerebral hypoperfusion/hypoxia — it is a change in level of consciousness, not anxiety, and it is the earliest sign.

What should you do first?

Stay with the patient and call for help / activate rapid response while you assess ABCs — because this patient is decompensating and cannot be left alone. Then in rapid sequence: oxygen if SpO₂ <90%, keep them flat or low-Fowler's, confirm IV access, 12-lead ECG and continuous monitoring, recheck BP, and anticipate fluids or inotropes/vasopressors per provider. Do NOT give nitroglycerin or morphine with a systolic of 82 — both drop preload and BP further.

🤖 Ask Claire: "Give me an unfolding MI case and reveal one clue at a time."

Not in the handout blanks, but she asks it every exam. Troponin is the answer to "which lab confirms MI?"

Serial draws: troponin is drawn on arrival and repeated (commonly at 3–6 hours, sometimes again at 12) — because a single early normal troponin does NOT rule out MI if the pain started less than 3 hours ago.

Test-taking trap: Normal troponin + chest pain 1 hour ago does not mean "no MI." Keep monitoring.

When the question says "a patient reports crushing chest pain — what does the nurse do FIRST?", this is the order.

Priority rule: Assessment before intervention, EXCEPT when the intervention is time-critical and standing-order driven. In practice: stay with the patient, get the ECG, give the aspirin — those three happen almost simultaneously.

Fill in the Blanks

• P wave = atrial depolarization — the electrical signal spreading through the atria, which triggers atrial contraction
• QRS complex = ventricular depolarization — the signal spreading through the ventricles, which triggers ventricular contraction (atrial repolarization is hidden inside it)
• T wave = ventricular repolarization — the ventricles electrically resetting/relaxing

Easy Memory Trick

P = Push (atria contract) · QRS = Squeeze (ventricles contract) · T = Time to recover (ventricles relax)

Normal intervals worth memorizing

• PR interval: 0.12–0.20 seconds (3–5 small boxes). Longer = AV block.
• QRS duration: 0.06–0.10 seconds (<0.12). Wide QRS = the beat came from the ventricles or conduction is blocked.
• Paper speed: 1 small box = 0.04 sec, 1 large box = 0.20 sec; count QRS complexes in a 6-second strip and multiply by 10 for the rate

Narrow QRS = the signal came from above the ventricles. Wide QRS = ventricular origin = worry.

🤖 Ask Claire: "Explain the P wave, QRS complex, and T wave in simple language and then quiz me with 5 questions."

Before naming any rhythm, ask the same four questions every single time.

Golden Rule ⭐

Treat the patient, not the monitor.

Think Like a Nurse 🧠

Telemetry shows VT. Before staring at the monitor, what should you check?

Go to the room and check the patient — responsiveness and a central (carotid) pulse. Because the entire treatment path splits on that one finding: pulse present → antiarrhythmics or synchronized cardioversion; no pulse → CPR and defibrillation. It may also be artifact from a loose lead or a shivering/brushing-teeth patient — but you confirm that at the bedside, not at the desk.

Defined as HR less than 60 bpm

Symptoms of poor perfusion: hypotension, dizziness/lightheadedness, syncope or near-syncope, confusion or restlessness, extreme fatigue and weakness, chest pain, shortness of breath, pale/cool/clammy skin, urine output <30 mL/hr

Medication commonly used if symptomatic: atropine 1 mg IV push, repeated every 3–5 minutes to a maximum total of 3 mg (2020 AHA dosing). If atropine fails → transcutaneous pacing, or a dopamine or epinephrine infusion.

Asymptomatic bradycardia is not treated — an athlete or a sleeping patient with HR 50 and warm, dry skin needs monitoring, not atropine.

⚠️ Atropine caution: it works at the AV node, so it is unreliable in Mobitz type II and third-degree (complete) heart block with a wide QRS — go straight to transcutaneous pacing in those.

Quick Question

Why can severe bradycardia cause confusion?

Cardiac output = heart rate × stroke volume. When the rate falls far enough, stroke volume cannot compensate, so cardiac output drops and the brain is under-perfused. Less oxygen to the cerebral cortex shows up first as restlessness, then confusion, then syncope. Confusion here is a perfusion sign, not a psych sign.

🤖 Ask Claire: "Create 5 symptomatic bradycardia cases and make me decide if atropine is appropriate."

Defined as HR greater than 100 bpm

Common causes

• Pain
• Fever
• Anxiety
• Hypovolemia / dehydration / hemorrhage (often the FIRST sign of blood loss)
• Hypoxia, anemia, infection/sepsis, hyperthyroidism
• Stimulants — caffeine, nicotine, cocaine, albuterol, epinephrine; also alcohol/drug withdrawal

Treatment

Treat the underlying cause — give analgesia for pain, antipyretics/cooling for fever, fluids for hypovolemia, oxygen for hypoxia, reassurance or anxiolytics for anxiety. Slowing the rate without fixing the cause removes the patient's compensation.

Remember

Sinus tachycardia is often the body's response to another problem. Why it still hurts the heart: a fast rate shortens diastole, and the coronary arteries fill during diastole — so the heart works harder on less blood.

🤖 Ask Claire: "Help me distinguish when tachycardia is compensatory versus when it is dangerous."

Hypertension means: persistently elevated arterial blood pressure. Per ACC/AHA: Normal <120/<80 · Elevated 120–129/<80 · Stage 1 130–139 or 80–89 · Stage 2 ≥140 or ≥90 · Hypertensive crisis >180 and/or >120. Diagnosis requires elevated readings on at least two separate occasions.

Major complications: stroke (hemorrhagic and ischemic), myocardial infarction and CAD, left ventricular hypertrophy → heart failure, chronic kidney disease/renal failure, retinopathy and vision loss, peripheral artery disease, and aortic aneurysm/dissection

Lifestyle Changes

• Diet: DASH pattern — fruits, vegetables, whole grains, low-fat dairy, lean protein; limit saturated fat
• Sodium: <2,300 mg/day, ideally 1,500 mg/day; read labels, avoid canned/processed/deli foods and salt substitutes containing potassium if on an ACE inhibitor or ARB
• Weight: lose excess weight — roughly 1 mmHg drop per kilogram lost
• Exercise: at least 150 minutes/week of moderate aerobic activity (about 30 min, 5 days a week)
• Alcohol / tobacco: limit alcohol to ≤2 drinks/day (men) or ≤1 (women); stop all tobacco and nicotine
• Other: stress management, adequate sleep, home BP monitoring, and — the big one — take the medication every day even when you feel fine

Think Like a Nurse 🧠

Why is hypertension often called the "silent killer"?

Because it produces no symptoms for years while it is damaging arteries, the heart, brain, kidneys, and eyes. Patients feel completely well, so they stop the medication — and the first "symptom" is often the stroke, MI, or kidney failure itself. Nursing implication: adherence teaching is the intervention.

🤖 Ask Claire: "Explain hypertension like I'm studying for the NCLEX and give me 5 practice questions."

Final Challenge

For every disease above, answer these four. Keep it short.

• What is the pathophysiology? Name the blocked or failing structure and what it stops doing — column 2 above.
• What assessment finding would make me most worried? Anything showing perfusion has failed: altered level of consciousness/restlessness, systolic <90, urine <30 mL/hr, cool clammy skin, a new lethal rhythm.
• What could kill the patient first? Airway → breathing → circulation, in that order. In cardiac patients it is almost always a lethal ventricular dysrhythmia or cardiogenic shock.
• What is my highest-priority nursing intervention? Stay with the patient, support ABCs, and get the one time-critical thing done — ECG, oxygen if hypoxic, defibrillation, or reperfusion.

Fill in the Blanks

• In atrial fibrillation, the atria quiver/fibrillate chaotically (multiple disorganized ectopic foci firing at 350–600/min) instead of contracting effectively.
• Because the atria do not empty well, blood can pool and stagnate — especially in the left atrial appendage — and form a thrombus.
• The biggest long-term complication is embolic stroke.

On the strip: no identifiable P waves (chaotic fibrillatory waves instead), irregularly irregular R–R intervals, usually a narrow QRS

Also loses the "atrial kick": the atrial contraction that normally tops off ventricular filling — losing it cuts cardiac output by roughly 20–30%, which is why patients feel fatigued, dizzy, and short of breath

Medications may be used to:

• Control the rate — beta blockers (metoprolol), calcium channel blockers (diltiazem), digoxin
• Control the rhythm — amiodarone, sotalol, flecainide; or synchronized cardioversion / ablation
• Prevent clots (stroke) — anticoagulants: warfarin (INR goal 2–3) or a DOAC such as apixaban or rivaroxaban

Never cardiovert A-fib lasting >48 hours without anticoagulation first — restoring organized contraction can launch an existing clot as a stroke.

Memory Trick

A-Fib = Atria Fibrillate → Blood Forms Clots → Stroke Risk

Think Like a Nurse 🧠

Your patient has A-fib and suddenly cannot move their right arm. What complication do you suspect?

Embolic (ischemic) stroke — a clot from the fibrillating left atrium traveled to the cerebral circulation. Priority: activate the stroke alert/rapid response, note the last known well time, perform a focused neuro exam, keep the patient NPO (swallow screen first), and prepare for an emergent non-contrast head CT to decide about thrombolytics.

🤖 Ask Claire: "Give me three A-fib cases and make me identify the priority complication."

Fill in the Blanks

• VT starts in the ventricles — an irritable ectopic focus below the bundle of His. Strip shows 3+ consecutive wide, bizarre QRS complexes at 100–250/min with no visible P waves.
• This rhythm can decrease cardiac output — the rate is too fast for the ventricles to fill and there is no atrial kick, so stroke volume and perfusion collapse.

If the patient has a pulse: Assess the patient's stability (pulse quality, blood pressure, level of consciousness, chest pain, shortness of breath) first.

If the patient has NO pulse: Start high-quality CPR (and call a code) and prepare for immediate defibrillation — unsynchronized shock — plus epinephrine 1 mg q3–5 min and amiodarone 300 mg after the third shock.

Think Like a Nurse 🧠

Why can VT quickly become fatal?

Because the ventricles are beating too fast to fill, cardiac output falls toward zero — and VT readily degenerates into ventricular fibrillation. Once there is no perfusion, brain injury starts within about 4–6 minutes. VT with a pulse can become VT without a pulse in seconds, so the patient needs continuous monitoring, IV access, and a defibrillator at the bedside.

Remember

No pulse = treat the patient, not just the rhythm.

• VF causes the ventricles to: quiver chaotically instead of contracting — totally disorganized electrical activity with no recognizable P wave, QRS, or T wave, just an erratic wavy baseline
• Cardiac output becomes: zero — there is no effective contraction, so the patient is pulseless, apneic, and unresponsive. This IS cardiac arrest.
• Priority treatment: immediate defibrillation (unsynchronized shock) with high-quality CPR before and immediately after each shock; then epinephrine 1 mg IV q3–5 min and amiodarone 300 mg after the third shock. Every minute without defibrillation drops survival by about 7–10%.

Quick Check

Can a patient in VF be awake?

• Yes — ❌ No. There is no cardiac output, so there is no cerebral perfusion.
• No — ✅ Correct. A VF patient is always pulseless and unresponsive.

So if the monitor shows VF and the patient is talking to you: it is artifact — a loose or disconnected lead, movement, shivering, or brushing teeth. Check the patient and the leads, never shock a talking patient.

🤖 Ask Claire: "Create five VF scenarios and ask me what I should do first."

• Asystole means: no electrical activity in the heart at all — a flat line. No contraction, no cardiac output, no pulse. Confirm it in two different leads and check that the leads are attached and the gain is up before calling it.

Should you defibrillate?

• Yes — ❌ No. Asystole is NOT a shockable rhythm.
• No — ✅ Correct. Defibrillation depolarizes electrical activity so the SA node can resume — with a flat line there is nothing to depolarize.

Treatment includes: immediate high-quality CPR, epinephrine 1 mg IV/IO every 3–5 minutes, airway management/ventilation, and searching for reversible causes (the H's and T's: hypoxia, hypovolemia, hydrogen ion/acidosis, hypo-/hyperkalemia, hypothermia; tension pneumothorax, tamponade, toxins, thrombosis — pulmonary or coronary).

Memory Trick

Flat line = CPR + epinephrine, not a shock.

Shockable vs. not — know this cold

Used for patients who have:

• A pulse — ✅ Yes. Cardioversion is for an unstable patient who still has a perfusing (but bad) rhythm.
• No pulse — ❌ No. A pulseless patient gets CPR and defibrillation instead.

Typical rhythms: unstable A-fib with RVR, atrial flutter, SVT, and VT with a pulse in a patient who is hypotensive, altered, or having chest pain

The shock is timed with the R wave of the QRS complex — the machine's "sync" button must be on and you must see sync markers on each R wave.

The patient often requires: sedation/analgesia (procedural sedation, e.g., midazolam ± an analgesic) plus informed consent, and — for A-fib lasting more than 48 hours — anticoagulation or a TEE beforehand

Think Like a Nurse 🧠

Why is cardioversion synchronized instead of delivered randomly?

To avoid delivering the shock on the T wave. The T wave is the relative refractory period — the heart's vulnerable window — and a shock landing there ("R-on-T") can throw the patient into ventricular fibrillation. Syncing to the R wave guarantees the energy lands on depolarization, not repolarization.

Used for: ventricular fibrillation and pulseless ventricular tachycardia — those two rhythms only

The patient is usually:

• Awake — ❌ No. If they are awake and perfusing, this is the wrong treatment.
• Pulseless — ✅ Yes. Unresponsive, pulseless, not breathing normally.

Nursing steps: continue compressions while the pads go on → select unsynchronized mode → charge → call "CLEAR!" and visually confirm no one (including you) is touching the patient or the bed → shock → resume compressions immediately for 2 minutes before rechecking the rhythm. Remove transdermal patches and do not place pads directly over an implanted device.

Remember

Defibrillation is an emergency treatment for life-threatening rhythms without effective circulation.

🤖 Ask Claire: "Compare synchronized cardioversion and defibrillation using patient scenarios."

A pacemaker helps treat: symptomatic bradycardia, sick sinus syndrome, second-degree (Mobitz II) and third-degree/complete heart block, and chronic bradydysrhythmias that do not respond to medication — it delivers an electrical impulse when the heart's own rate falls below the set rate

Patient Teaching

• Carry your: pacemaker identification card at all times (device type, model, settings, manufacturer), and wear a medical-alert bracelet
• Report: a pulse rate BELOW the set rate; dizziness, fainting, or new palpitations; hiccups or muscle twitching; shortness of breath, chest pain, or swelling; and redness, swelling, drainage, or fever at the incision site. Check and record your own pulse daily.
• Avoid: MRI (unless the device is MRI-conditional), arc welding, large industrial magnets, diathermy, and TENS units; no heavy lifting or raising the arm above the shoulder on that side for about 4–6 weeks; no contact sports; keep cell phones at least 6 inches away and use the opposite ear; walk briskly through antitheft/security gates rather than lingering. Microwaves are safe.

Think Like a Nurse 🧠

A patient reports hiccups after pacemaker insertion. Why should the nurse notify the provider?

Persistent hiccups (or chest-wall twitching) suggest the pacing lead has migrated or dislodged and is now stimulating the diaphragm or phrenic nerve. A displaced lead means the pacemaker may not be capturing the ventricle — so the patient can drop back into symptomatic bradycardia. It is an early, easy-to-dismiss sign of device failure and needs a chest x-ray and interrogation.

Purpose: to continuously monitor the rhythm and automatically terminate life-threatening ventricular dysrhythmias (VT/VF) — it is implanted in patients at risk for sudden cardiac death, such as survivors of cardiac arrest, sustained VT, or an ejection fraction ≤35%

The device can:

• Pace the heart
• Detect dangerous rhythms
• Deliver a shock (antitachycardia pacing, then synchronized cardioversion or defibrillation) if needed

Teaching

• Inform healthcare providers before: any MRI, surgery, electrocautery, diathermy, radiation therapy, or lithotripsy — and tell airport/store security about the device
• Avoid placing: cell phones, strong magnets, MP3 players, or tight straps/shoulder bags directly over the device.

Quick Check

If the AICD fires, should the patient notify their provider?

• Yes — ✅ Correct. Every firing means the device detected a lethal rhythm — the provider needs to interrogate the device.
• No — ❌ Wrong. "It worked, so I'm fine" is exactly the thinking that gets a patient into trouble.

How to teach it: one shock and you feel fine → call the provider that day. Multiple shocks, or a shock with chest pain, dizziness, or shortness of breath → call 911. Bystanders touching the patient during a discharge may feel a harmless tingle — that is not dangerous. Do not drive until cleared.

PCI (Stent)

• Purpose: to open the blocked coronary artery and restore blood flow — a catheter (usually radial or femoral) is threaded to the lesion, a balloon inflates, and a stent holds the vessel open. For STEMI the goal is door-to-balloon within 90 minutes.
• After the procedure, assess: the insertion site for bleeding, hematoma, or swelling; distal pulses, color, temperature, capillary refill, and sensation in that extremity; vital signs and cardiac rhythm (reperfusion dysrhythmias); recurrent chest pain, which may mean the vessel re-occluded; and urine output/renal function because of the contrast dye. Keep the extremity straight, maintain bedrest per protocol, and encourage fluids to flush the contrast.

CABG

• Purpose: to bypass the blockage by grafting a new vessel around it — used for left main disease, multi-vessel disease, or lesions PCI cannot fix. It reroutes blood; it does not remove the plaque.
• A graft may come from the: internal mammary (internal thoracic) artery in the chest — the best long-term patency; the greater saphenous vein from the leg; or the radial artery from the forearm

Think Like a Nurse 🧠

Why is checking the incision and circulation important after these procedures?

Because the two things most likely to kill this patient early are bleeding and loss of perfusion. These patients are on antiplatelets and anticoagulants, so a puncture site or sternal/leg incision can bleed or form an expanding hematoma fast — and retroperitoneal bleeding after a femoral stick may show up only as back pain and falling BP. Checking pulses, color, temperature, and sensation distal to the site tells you whether the artery is still open or has clotted/occluded. The incision also tells you early about infection.

🤖 Ask Claire: "Create a patient scenario after PCI and another after CABG. Ask me what complication I should monitor for."

Match the Condition to the Biggest Danger

Prioritization Practice

Mini Case Study

One-Minute Review

• CAD — Blocked artery → less oxygen to the heart muscle (ischemia → chest pain)
• Stable Angina — Pain with activity → relieved by rest and sublingual nitroglycerin
• MI — Heart muscle begins to die (necrosis — irreversible)
• A-Fib — Biggest complication = stroke
• Bradycardia — Symptomatic treatment may include atropine, then transcutaneous pacing
• Pulseless VT — Treat with CPR + defibrillation
• VF — Treat with CPR + defibrillation
• Asystole — Treat with CPR + epinephrine (no shock)
• Pacemaker — Used for symptomatic bradycardia and heart block (too slow)
• AICD — Protects against dangerous ventricular rhythms — VT and VF (too fast/lethal)
• PCI — Opens blocked coronary arteries (balloon + stent)
• CABG — Creates a new route for blood flow around the blockage, using a grafted artery or vein

🤖 Favorite prompt: "Claire, act like an experienced cardiac ICU nurse and ATI instructor. Give me one patient scenario at a time. Don't ask me for the diagnosis first — ask me: (1) What assessment finding worries you the most? (2) What could kill this patient first? (3) What should the nurse do next? Then explain the reasoning and the pathophysiology."

1. Stable = predictable, relieved by rest and nitro. Unstable = at rest, unrelieved, and it is an emergency. Unstable angina is ACS.
2. UA vs NSTEMI = troponin. NSTEMI vs STEMI = ST elevation. Troponin rises in 3–4 hours, peaks 10–24 hours, stays up 7–14 days — so it is drawn serially.
3. Chest pain order: stay with the patient → 12-lead ECG within 10 minutes → chewed aspirin → O₂ only if SpO₂ <90% → nitro (check BP) → troponin → reperfusion. STEMI: PCI ≤90 min.
4. Nitroglycerin: 0.4 mg SL q5min ×3, sit down first, hold if SBP <90, never with sildenafil/tadalafil, and call 911 if pain persists 5 minutes after the first dose.
5. Shockable = VF and pulseless VT only. Asystole and PEA get CPR + epinephrine. Never defibrillate a flat line.
6. Cardioversion = has a pulse, synced to the R wave, sedate first. Defibrillation = pulseless, unsynchronized, go now.
7. A-fib → clot → stroke. Rate control, rhythm control, and anticoagulation — and never cardiovert >48-hour A-fib without anticoagulation.
8. Treat the patient, not the monitor. The first assessment for any bad rhythm is responsiveness, pulse, BP, and level of consciousness — restlessness and urine <30 mL/hr are your earliest perfusion failures.