Every blank from the Module 8 handout, filled in. Tap "Hide answers" to quiz yourself.
Directions from the handout: complete these while reviewing ATI and lecture. Keep answers short. If something doesn't click, ask Claire for another practice scenario.
| Valve problem | What you hear / see | What it leads to |
|---|---|---|
| Mitral stenosis | Rumbling diastolic murmur, loud S1, dyspnea, hemoptysis | Left atrium enlarges → atrial fibrillation → clot → stroke; pulmonary congestion |
| Aortic stenosis | Harsh systolic murmur; classic triad = angina, syncope, exertional dyspnea | Left ventricular hypertrophy → left-sided heart failure → sudden death with exertion |
| Mitral regurgitation | Blowing systolic murmur at the apex | Blood pushed backward into the left atrium and lungs → pulmonary congestion, afib |
| Aortic regurgitation | Blowing diastolic murmur, widened pulse pressure, bounding pulses | Left ventricle volume-overloads and dilates → left-sided heart failure |
Memory: Systolic murmurs = Aortic Stenosis + Mitral Regurg (SAS-MR). Diastolic = the other two.
A client says, "I get tired just walking to the mailbox." What body system is not getting enough blood flow?
The systemic circulation — the whole body, and especially the skeletal muscles. The damaged valve drops stroke volume, so cardiac output can't rise to meet the oxygen demand of walking, and she fatigues. Fatigue with ordinary activity is an early sign of falling cardiac output, not "just deconditioning."
Easy Memory Trick (from the handout): Bad valve = bad flow = heart works harder.
🤖 Ask Claire: "Explain stenosis versus regurgitation in simple terms and give me two NCLEX questions."
Why does climbing stairs become difficult for these patients?
Climbing stairs raises oxygen demand, so the heart must push more blood through the lungs. The pulmonary vessels are stiff and narrowed, so the right ventricle cannot increase output against that resistance. Less blood reaches the left heart → cardiac output stays flat → dyspnea, fatigue, and sometimes syncope with exertion.
Remember: Pulmonary hypertension stresses the RIGHT side of the heart.
Common findings:
Common findings:
| Drug class | Nursing point |
|---|---|
| ACE inhibitors (–pril) | Watch for dry cough, angioedema, hyperkalemia, first-dose hypotension |
| ARBs (–sartan) / ARNI | Used when the ACE cough is intolerable; still causes hyperkalemia. Entresto requires a 36-hour washout from an ACE inhibitor. |
| Beta blockers (carvedilol, metoprolol succinate) | Start low, go slow; hold and reassess if apical pulse <50–60 or systolic BP is low. Never stop abruptly — rebound tachycardia and ischemia. |
| Loop diuretics (furosemide) | Best sign it worked = weight loss and increased urine output. Monitor for hypokalemia, hyponatremia, orthostatic hypotension, ototoxicity with rapid IV push. |
| Spironolactone | Potassium-sparing → risk of hyperkalemia; teach to avoid salt substitutes (they are potassium chloride) |
| Digoxin | Take apical pulse for a full minute; hold if <60 and notify. Therapeutic level 0.5–2 ng/mL. Toxicity = anorexia, nausea, vomiting, visual halos / yellow-green vision, bradycardia. Hypokalemia potentiates toxicity — so a patient on furosemide + digoxin is the high-risk one. |
A patient has crackles and cannot lie flat. Which side of the heart is likely failing?
The LEFT side. Crackles and orthopnea mean fluid is backing up into the lungs, which is what happens when the left ventricle can't move blood forward. Priority action: raise the head of the bed, apply oxygen, and recheck SpO₂ — because oxygenation comes before anything else.
🤖 Ask Claire: "Create three heart failure cases where I decide if it is left-sided or right-sided."
If you remember nothing else: LEFT = LUNGS. RIGHT = REST OF THE BODY.
| LEFT-sided HF | RIGHT-sided HF | |
|---|---|---|
| Where does blood back up? | Backward into the pulmonary veins and lungs | Backward into the systemic venous system — neck, liver, abdomen, legs |
| Most common cause | Hypertension, MI/CAD, aortic or mitral valve disease | Left-sided failure is the #1 cause; then cor pulmonale from COPD or pulmonary hypertension |
| Hallmark assessment finding | Crackles + orthopnea | JVD + dependent pitting edema |
| Respiratory findings | Dyspnea, PND, cough, frothy sputum, ↓ SpO₂ | Usually clear lungs unless the left side is failing too |
| GI / abdominal | Generally none | Hepatomegaly, ascites, RUQ pain, anorexia and nausea |
| Heart sound | S3 gallop (volume overload) | Right-sided S3/S4, and a murmur if tricuspid regurgitation develops |
| Weight gain / edema | Weight gain from pulmonary congestion; less visible peripheral edema early | Obvious weight gain, ankle/sacral edema, growing abdominal girth |
| What kills first | Flash pulmonary edema → hypoxemic respiratory failure | Progressive low output, liver congestion, and worsening hypoxemia from the underlying lung disease |
| Priority nursing action | High Fowler's, oxygen, loop diuretic, monitor SpO₂ — fix oxygenation first | Daily weights, strict I&O, sodium/fluid restriction, assess edema and abdominal girth |
Why legs dependent? It pools blood in the legs and reduces venous return, so less volume arrives at the already-flooded lungs.
Never lay a patient with pulmonary edema flat — it dumps more blood into the lungs and can arrest them.
Why is pulmonary edema a medical emergency?
Because the alveoli are filling with fluid, oxygen physically cannot cross into the blood. Hypoxemia gets worse by the minute and progresses to respiratory failure and cardiac arrest. It is an airway/oxygenation problem, so it outranks every other need on your patient list.
Remember: Fluid in the lungs = oxygen cannot get where it needs to go.
| Type | What's wrong | Key nursing point |
|---|---|---|
| Dilated (most common) | Ventricles stretch out and become floppy → low ejection fraction | Treat like systolic heart failure; avoid alcohol (a common cause); anticoagulation for clot risk in the dilated chamber |
| Hypertrophic (HCM) | Thickened septum obstructs outflow; the stiff ventricle can't fill. The young athlete who collapses during a game. | Avoid strenuous exercise, dehydration, and Valsalva. Avoid nitrates, diuretics, and positive inotropes — they shrink the ventricle and worsen the obstruction. Beta blockers or verapamil are used. Screen first-degree relatives. |
| Restrictive (rarest) | Stiff, non-compliant walls that cannot fill during diastole; EF may be normal | Looks like right-sided failure — JVD, ascites, edema. Treat the underlying cause (amyloidosis, sarcoidosis). |
Why might these patients develop heart failure?
Because the pump muscle itself is damaged. If it can't contract (dilated) or can't fill (hypertrophic/restrictive), stroke volume and cardiac output fall, so blood backs up behind the failing chamber — into the lungs, the body, or both. Cardiomyopathy is a direct road to heart failure and to lethal dysrhythmias, which is why many of these patients get an ICD.
🤖 Ask Claire: "Explain cardiomyopathy like I'm studying for ATI and give me three practice questions."
| Disease | Biggest Problem | Nurse Worries About |
|---|---|---|
| Valve Disorder | Blood cannot move forward normally — it is either blocked (stenosis) or leaks backward (regurgitation), so cardiac output falls | Heart failure, atrial fibrillation with clot → stroke, infective endocarditis, activity intolerance and syncope |
| Pulmonary HTN | High pressure in the pulmonary arteries forces the right ventricle to pump against resistance it cannot beat | Right-sided heart failure (cor pulmonale), worsening hypoxemia, exertional syncope, sudden death |
| Left HF | Blood backs up into the lungs — pulmonary congestion | Crackles, orthopnea, falling SpO₂, and a flip into acute pulmonary edema |
| Right HF | Blood backs up into the systemic venous circulation — the rest of the body | JVD, pitting edema, rapid weight gain, ascites and liver congestion, poor nutrition from GI congestion |
| Pulmonary Edema | The alveoli flood, so gas exchange stops | Severe hypoxemia → respiratory failure and arrest — a true emergency, minutes matter |
| Cardiomyopathy | The heart muscle itself is diseased, so it cannot contract or cannot fill | Low cardiac output, lethal dysrhythmias and sudden cardiac death, clot formation, progression to end-stage heart failure |
Your patient suddenly develops: RR 34 · SpO₂ 84% · crackles · pink frothy sputum · severe anxiety.
What complication is occurring?
Acute pulmonary edema from decompensated left-sided heart failure. Pink frothy sputum plus crackles plus an SpO₂ of 84% is that picture and nothing else. The "severe anxiety" is air hunger, not a psychiatric symptom — never treat sudden anxiety in a cardiac patient as anxiety until you have ruled out hypoxia.
What should the nurse do first?
Sit the patient straight up (high Fowler's) with the legs dangling and apply high-flow oxygen by non-rebreather — because oxygenation is failing right now, and position plus oxygen are the two things the nurse can do in the first ten seconds without an order. Then call the rapid response team, get the provider, and anticipate IV furosemide, nitroglycerin, a cardiac monitor, and possible BiPAP.
🤖 Claire Challenge: "Create five ATI-style questions about heart failure and pulmonary edema that focus on recognizing the patient who is deteriorating."
Why can myocarditis decrease cardiac output?
Inflamed, swollen myocardium contracts weakly, so stroke volume drops — and cardiac output = stroke volume × heart rate. The inflammation also irritates the conduction system, causing dysrhythmias that reduce filling time. Severe cases progress to dilated cardiomyopathy, heart failure, or sudden death.
How is pericarditis pain different from an MI?
Position and breathing change pericarditis pain; nothing changes MI pain. Pericarditis: sharp, stabbing, pleuritic, worse lying flat and with inspiration, better sitting forward, friction rub present, diffuse ST elevation, troponin normal or only mildly up. MI: crushing pressure or squeezing, radiates to jaw/left arm/back, constant regardless of position or breathing, associated with diaphoresis and nausea, ST elevation only in the leads over the infarct, troponin clearly rising.
Memory Trick: Lean forward = pain improves.
Pericarditis → pericardial effusion → tamponade. Fluid in the sac squeezes the heart so it cannot fill.
Notify the provider immediately and prepare for pericardiocentesis — because removing even 20–50 mL of fluid restores filling and output within seconds. Meanwhile: high Fowler's, oxygen, IV fluids to support preload, continuous monitoring. Never assume a hypotensive pericarditis patient just needs "more time on the diuretic" — hypotension + JVD together is tamponade until proven otherwise.
They identify the organism causing the infection so the right antibiotic can be chosen — usually Streptococcus viridans or Staphylococcus aureus. Draw at least two to three sets from different sites before the first antibiotic dose, because one dose can make the culture negative and leave the team guessing. Treatment is 4–6 weeks of IV antibiotics, often at home through a central line.
🤖 Ask Claire: "Compare myocarditis, pericarditis, and endocarditis using simple patient cases."
| Myocarditis | Pericarditis | Endocarditis | |
|---|---|---|---|
| Layer involved | Middle layer — the muscle | Outer sac around the heart | Inner lining and the valves |
| Usual cause | Viral infection | Viral illness, post-MI (Dressler's), uremia, cardiac surgery | Bacteria in the bloodstream landing on a damaged valve |
| Signature finding | Fatigue and dyspnea after a viral illness, tachycardia, rising troponin | Friction rub; pain better leaning forward | Fever + new murmur + splinter hemorrhages / Osler nodes |
| Key test | Echocardiogram + troponin; endomyocardial biopsy if needed | ECG with diffuse ST elevation; echo to look for effusion | Blood cultures × 2–3 sets + echo (TEE) for vegetations |
| Feared complication | Dilated cardiomyopathy, heart failure, lethal dysrhythmia | Cardiac tamponade | Embolism — vegetation breaks off → stroke, splenic/renal infarct, PE; plus valve destruction → heart failure |
| Core treatment | Rest, treat heart failure, monitor rhythm | NSAIDs + colchicine; pericardiocentesis if tamponade | 4–6 weeks IV antibiotics; valve surgery if destroyed |
Rest — and with the legs in a dependent position (dangling off the bed), because gravity helps pull arterial blood down into the leg. Later-stage PAD hurts at rest too, and those patients often sleep in a chair.
Memory Trick: PAD = Pain with Activity.
Elevating the legs above heart level and with walking and compression stockings — because gravity and the calf-muscle pump help push pooled blood back toward the heart. It gets worse with prolonged standing or sitting with the legs down.
| PAD (arterial) | PVD (venous) | |
|---|---|---|
| Pain pattern | With activity, relieved by rest and dangling | Dull ache after standing all day, relieved by elevation |
| Skin | Pale, shiny, hairless, cool, thick nails | Brown/bronze stained, warm, edematous |
| Pulses | Weak or absent | Present (may be hard to palpate through edema) |
| Ulcer location / look | Toes, heels, lateral malleolus — deep, round, punched-out, very painful, minimal drainage | Medial malleolus — shallow, irregular edges, heavy drainage, less painful |
| Position the legs | DOWN (dependent) | UP (elevated) |
| Compression stockings? | ❌ No — dangerous in arterial disease | ✅ Yes — the mainstay of treatment |
Pulmonary embolism — the clot breaks loose, travels through the right heart, and lodges in the pulmonary artery. Signs: sudden dyspnea, pleuritic chest pain, tachycardia, tachypnea, hypoxemia, anxiety with a sense of impending doom, sometimes hemoptysis. Action: raise the head of the bed, give oxygen, call rapid response, stay with the patient. The long-term complication is chronic venous insufficiency (post-thrombotic syndrome).
Why should you avoid massaging the affected leg?
Because rubbing the leg can dislodge the clot and send it to the lungs as a pulmonary embolism. Same reason you don't do vigorous calf exercises or check a Homans sign on a known DVT. Teach the patient and the family not to rub the leg.
🤖 Ask Claire: "Create five DVT scenarios where I identify who is at greatest risk for pulmonary embolism."
Why is rupture life-threatening?
The aorta carries the body's entire cardiac output. When it tears, the patient bleeds internally at enormous speed — liters in minutes — and goes into hypovolemic shock before anyone can see external blood. Action: notify the surgical team / call a code, large-bore IVs, type and crossmatch, keep NPO, prepare for emergency surgery. Mortality without immediate surgery is near total.
Memory Trick: Aneurysm ruptures = internal bleeding until proven otherwise.
Post-op after AAA repair: check peripheral pulses and extremity color/temperature hourly (graft occlusion), monitor urine output ≥30 mL/hr (renal perfusion), watch for abdominal distention and back pain (bleeding), keep BP in the ordered range — too high stresses the graft, too low clots it.
| Disease | Biggest Danger |
|---|---|
| PAD | Critical limb ischemia — tissue dies from lack of arterial flow, leading to non-healing ulcers, gangrene, and amputation. An acute occlusion (the 6 Ps) is a limb-threatening emergency. |
| PVD | Venous stasis ulcers that will not heal, with cellulitis and infection on top of them — chronic disability rather than sudden death. |
| DVT | Pulmonary embolism — sudden, and it can kill in minutes. |
| Raynaud | Prolonged vasospasm → fingertip ulceration and gangrene with permanent tissue loss. |
| Aortic Aneurysm | Rupture → massive internal hemorrhage → hypovolemic shock and death. |
Not printed in the Module 8 handout, but it is on Exam 3 and it is the single most common "what do you do first" question. Learn the decision, not the squiggles.
| Defibrillation | Synchronized cardioversion | |
|---|---|---|
| Used for | VF and pulseless VT — no pulse | Unstable with a pulse: SVT, atrial fib/flutter with RVR, VT with a pulse |
| Timing | Unsynchronized — fires the instant you press the button | Synced to the R wave, so it will not fire during the T wave — a shock on the T wave can cause VF |
| Sedation | None — the patient is unresponsive | Yes, sedate first when there is time (the patient is awake) |
| Nurse safety | "I'm clear, you're clear, everybody clear" — look before you shock, oxygen away from the bed, no one touching the patient or the bed. | |
Never delay defibrillation in VF to start an IV, intubate, or find a doctor — survival drops roughly 7–10% for every minute without a shock.
Formula: Desired ÷ Have × Quantity = Amount to Give
How many mL? 40 mg ÷ 20 mg × 1 mL = 2 mL. Push slowly — no faster than 20 mg/min — because rapid IV furosemide causes ototoxicity.
How many tablets? 50 mg ÷ 25 mg × 1 tab = 2 tablets. Check the apical pulse and BP first; hold and notify if the pulse is under 60 or the systolic BP is below the ordered parameter.
How many mL? 5,000 units ÷ 10,000 units × 1 mL = 0.5 mL. Heparin is a high-alert drug — independent double-check with a second nurse before giving.
For every disease in this module: What is happening? What finding worries you most? What could kill the patient first? What should the nurse do first?
| Disease | What's happening | Finding that worries you most | Nurse's FIRST action |
|---|---|---|---|
| Left HF | Left ventricle can't move blood forward, so it backs into the lungs | New crackles with falling SpO₂ and orthopnea | High Fowler's + oxygen, then reassess |
| Right HF | Right ventricle fails, blood backs into the body | Weight gain >2–3 lb in 24 hours with JVD | Assess (weight, lungs, edema, vitals) and notify the provider |
| Pulmonary edema | Alveoli flood — gas exchange stops | Pink frothy sputum with SpO₂ in the 80s | Sit upright with legs dependent + high-flow oxygen, call rapid response |
| Tamponade | Fluid in the pericardial sac stops the heart from filling | Beck's triad: hypotension + JVD + muffled heart sounds | Notify the provider and set up for pericardiocentesis |
| Endocarditis | Bacteria colonize a valve and grow vegetations | Fever + a new murmur, or sudden focal neuro change (embolic stroke) | Blood cultures before antibiotics, then give the antibiotic on time |
| DVT | Clot in a deep leg vein | Sudden dyspnea and pleuritic chest pain = PE | Raise the head of the bed, oxygen, call rapid response, do not massage the leg |
| Aortic aneurysm | Weakened aortic wall balloons out | Sudden tearing back/abdominal pain with hypotension | Call for emergency surgical help, large-bore IV access, type and crossmatch, NPO |
| VF / pulseless VT | The ventricles quiver instead of pumping — no cardiac output | Unresponsive with no pulse | Start CPR and defibrillate as soon as the pads are on |
🤖 Final Claire Challenge: "Act like an ATI tutor and give me 10 difficult cardiovascular cases involving valve disorders, heart failure, DVT, PAD, pulmonary edema, and aneurysms. Make me identify the biggest red flag and the nurse's first action before revealing the answer."