1.1 Coronary Anatomy — Why the Map Matters

Every question about infarct location traces back to one fact: each coronary artery feeds a specific region of myocardium. When an artery occludes, the muscle downstream of the blockage becomes ischemic, then necrotic. Learn which artery feeds which wall now and the 12-lead section later becomes recognition instead of memorization.

• Left anterior descending (LAD) — anterior wall and interventricular septum. The largest territory, sometimes called the widow-maker.
• Left circumflex — lateral wall of the left ventricle.
• Right coronary artery (RCA) — inferior wall. (Background worth carrying, though it is not on her slides: the RCA also feeds the SA and AV nodes in most people, which is why inferior MI so often arrives with bradycardia and AV block.)

1.2 Coronary Artery Disease and Atherosclerosis

CAD is the most common cardiovascular disease and the leading cause of death in the United States. It sits in the category of atherosclerosis — lipid deposits forming within the tunica intima, the innermost layer of the artery wall.

The step that starts everything is endothelial injury. A layer of endothelial cells normally sits between the intima and the blood, keeping substances out of the wall that do not belong there. Damage that barrier and lipoproteins can carry cholesterol from the blood into the intima, where plaque begins.

The three stages of CAD

1.3 Risk Factors

Metabolic syndrome

Also called syndrome X. A cluster of conditions occurring together that raises the risk of heart disease, stroke, and type 2 diabetes: increased blood pressure, high blood sugar, excess body fat around the waist, and abnormal cholesterol and triglyceride levels.

1.4 Collateral Circulation

Named explicitly on the posted exam study guide. Collateral circulation is arterial anastomoses — new connections that develop around a blockage so blood has an alternate path to the tissue beyond it. The instructor's framing: think of it as a detour.

1.5 Nursing Management of CAD

• Identify patients at high risk — take an adequate health history covering family history, diabetes, hypertension, and smoking.
• Assess educational background and health literacy so teaching lands. Do not use dense medical terminology with a patient who cannot follow it.
• Educate on managing modifiable risk factors and developing health-promoting behaviors.
• Medication compliance and education.
• Help the patient set realistic goals. The instructor calls this one of the most important things — telling someone to exercise six or seven days a week and overhaul their diet at once is overwhelming and does not stick. Smaller, reachable goals produce consistency.

1.6 The ACS Taxonomy — Hold This Structure

Almost every ACS question depends on knowing where a presentation sits in this hierarchy. CAD is the umbrella term. Underneath it, one branch is chronic stable angina; the other is acute coronary syndrome, which contains unstable angina, NSTEMI, and STEMI.

1.7 Chronic Stable Angina

Myocardial demand for oxygen exceeds the ability of the coronary arteries to supply it. The result is myocardial ischemia, which the patient experiences as chest pain. The narrowing is fixed, so the pain is predictable — the same character, onset, and duration each time, brought on by the same triggers and relieved when the trigger is removed.

How patients actually describe it

• Often not called chest pain at all — pressure, heaviness, discomfort, squeezing, tightness, a suffocating sensation, or something sitting on the chest.
• Dyspnea and fatigue.
• No change with position or breathing — this is what separates it from pleuritic or musculoskeletal pain.
• Usually substernal, radiating to neck, jaw, shoulders, or arms; may present between the shoulder blades (interscapular).
• May be described as indigestion or epigastric burning.
• Lasts a few minutes and resolves once the aggravating factor is gone.
• Assess it with LOUDCARTS, the mnemonic on her slide.

Precipitating factors

EKG in chronic stable angina

ST segment depression and/or T wave inversion — the signature of ischemia without infarction. It resolves once oxygen supply is restored. Goals of treatment are simple and worth memorizing as a pair: reduce angina symptoms, and reduce the risk of MI and death.

1.8 Silent Ischemia

• Ischemia occurring without subjective symptoms.
• Seen in patients with diabetes mellitus, because neuropathy affects the nerves innervating the cardiovascular system. More likely in advanced diabetes where neuropathy has developed as a complication.
• EKG changes still appear — ST depression and/or T wave inversion. The ischemia is silent to the patient, not to the monitor.

1.9 Prinzmetal's Angina

A rare form occurring at rest, with no physical exertion, caused by hyperactivity of vascular smooth muscle producing spasm of the vessel. It can occur with or without CAD.

• Risk factors: history of migraines, Raynaud's phenomenon, heavy smoking.
• Substances and drugs: alcohol, cocaine, sumatriptan (which narrows blood vessels — hence the migraine link).
• EKG: transient ST segment elevation — it appears and then goes away.
• Patients may report short bursts of chest pain at the same time each day.
• Treatment: calcium channel blockers and sublingual nitroglycerin; remove the offending agent. Pain may also resolve spontaneously when the spasm stops.
• Long-acting nitrates are also used for Prinzmetal's.

1.10 Unstable Angina

A previously stable chronic plaque becomes unstable. It ruptures, releasing its lipid core into the vessel; platelets aggregate and a thrombus forms, partially or completely occluding the vessel. Partial occlusion produces unstable angina or NSTEMI; complete occlusion produces STEMI.

• Pain is new in onset and occurs at rest, not only with activity.
• In a patient with known chronic stable angina, the warning sign is a change in their normal pattern — increasing frequency, increasing duration, or a different character. They know their usual pain; when they say this one is different, listen.
• Lasts 10 minutes or more.
• EKG: ST depression and/or T wave inversion.
• Needs to be treated immediately.

1.11 NSTEMI and Cardiac Biomarkers

A myocardial infarction is the abrupt stoppage of blood flow in a vessel caused by platelet aggregation, blocking blood and oxygen to the heart. Everything downstream of the blockage becomes necrotic — irreversible myocardial cell death. In NSTEMI the occlusion is not complete, so the EKG may or may not show ST depression or T wave inversion in the leads facing the infarct.

1.12 STEMI

An occlusive thrombus completely blocks the vessel, producing ST elevation in the leads facing the infarcted area. This is an emergency.

Contiguous leads means two leads looking at the same region of the heart. For an inferior STEMI, the elevation must appear in two of II, III, and aVF.

1.13 Locating the Infarct

Named on the posted exam study guide as "location of myocardial infarction." The leads showing elevation tell you which wall is infarcting, which tells you which artery is occluded.

1.14 Percutaneous Coronary Intervention

First-line treatment for confirmed STEMI, with the goal of opening the blocked artery within 90 minutes of presentation at a PCI-capable hospital. Cardiac catheterization assesses the location and extent of the blockage; a guidewire is advanced from the femoral or radial artery to the coronary vessel, a balloon is inflated to push the plaque aside, and in most cases a stent is placed to hold the artery open.

Antiplatelet and anticoagulation after PCI

• Stents are thrombogenic — clots form on them.
• During PCI: unfractionated heparin or low molecular weight heparin (enoxaparin / Lovenox).
• After PCI: dual antiplatelet therapy (DAPT) — aspirin plus clopidogrel (Plavix).
• Aspirin for life. Clopidogrel for 12 months — or only 3–6 months with newer-generation drug-eluting stents.
• DAPT continues until the intimal lining grows over the metal stent, restoring a smooth surface for blood flow.

Benefits and complications

Nursing care after PCI

Named specifically on the posted exam study guide.

• Monitor vital signs and compare against baseline.
• Listen to heart and breath sounds.
• Assess neurovascular status of the affected extremity every 15 minutes for the first hour, then per agency policy — that is four checks in the first hour. Check distal to the site: pedal and posterior tibial pulses, capillary refill, temperature, color.
• Assess the catheter insertion site for hematoma, bleeding, and bruit.
• Place a compression device over the arterial site to achieve hemostasis, per agency policy.
• Monitor the ECG for dysrhythmias.
• Monitor for chest pain. Pain should be relieved after PCI. If it is not, the patient may have another blockage or the PCI may have failed — report to the provider right away.
• Teach the patient and caregiver about discharge medications.

1.15 Thrombolytic Therapy

Indicated when the patient is at a facility without PCI capability. These drugs break up the fibrin meshwork in the clot, dissolving the occlusive thrombus and restoring perfusion.

The instructor answered a class question about these drugs: yes, thrombolytics from this same group are what the ED uses for ischemic stroke — never hemorrhagic, since that patient is already bleeding. (The specific agent she named is garbled in the recording, so it is left unnamed here rather than guessed at; alteplase and tenecteplase are both used for stroke.)

Absolute contraindications

She read these aloud from the textbook chart. The common thread is simple — anything that means the patient is bleeding, has bled into the head, or is about to.

• Active internal bleeding
• History of intracranial hemorrhage
• Intracranial or intraspinal surgery within 2 months
• Known structural or vascular abnormality (e.g. arteriovenous malformation)
• Known intracranial cancer, primary or metastatic
• Ischemic stroke within the past 3 months
• Severe uncontrolled hypertension
• Significant closed-head or facial trauma within the past 3 months
• Suspected aortic dissection

Nursing points during and after

• Place 2–3 IV lines and draw baseline labs before starting; complete all other invasive procedures first, to reduce bleeding risk.
• The most reliable sign of reperfusion is return of the ST segment to baseline. Others: resolution of chest pain, and an early rapid rise in cardiac biomarkers as the necrotic cells wash out.
• Reperfusion dysrhythmias are common and generally self-limiting.
• Main complication is bleeding. Assess neurologic status regularly for signs of cerebral bleeding.
• Reocclusion is a major concern — IV heparin is started, and the patient should be moved to a PCI-capable facility.

1.16 Coronary Artery Bypass Graft

The posted exam study guide asks two things about CABG: when it is indicated, and nursing care after surgery.

The procedure

• Sternotomy — the chest is opened down the middle and the ribs moved to reach the heart.
• Cardiopulmonary bypass — the heart is stopped and a machine oxygenates and circulates the blood, doing the work of the heart and lungs.
• Most common conduit: the left internal mammary artery (LIMA), which comes off the subclavian artery and is closest to the heart.
• Alternatives: saphenous vein from the leg, or radial artery from the forearm.
• Off-pump CABG — still a sternotomy, but performed on a beating heart using mechanical stabilizers, so no bypass machine is needed.

Post-operative care

• ICU stay for 24–48 hours.
• Most patients extubated within about 6 hours.
• Transferred to step-down in 24–48 hours if stable.
• Monitor hemodynamics — BP, HR, and the invasive lines.
• Expect a full inventory of lines: arterial line for continuous BP, pleural and/or mediastinal chest tubes, continuous ECG, endotracheal tube, epicardial pacing wires, Foley catheter, possible NG tube for gastric decompression.

Complications — mostly from the bypass machine

Nursing management after CABG

• Assess for bleeding from the chest tube and incision site.
• Monitor hemodynamics and check fluid status.
• Replace blood and electrolytes as ordered.
• Restore temperature with warming blankets.
• Wound care to the incision site.
• Manage pain — the chest was cut open, and uncontrolled pain prevents deep breathing.
• Prevent VTE — sequential compression devices and early ambulation.
• Prevent respiratory compromise — incentive spirometry, deep breathing, and coughing to expand the alveoli and prevent atelectasis and pneumonia.

1.17 The Patient Arriving With Chest Pain

A high-yield sequence, because it is naturally written as a "which action would the nurse take first" question.

1.18 Drug Therapy for Angina and MI

Nitrates

The other drug classes

How calcium channel blockers work, from first principles. Calcium normally causes vasoconstriction of arterial smooth muscle and drives cardiac contraction — whenever calcium enters, muscle excites, contracts, and constricts. Blocking calcium entry relaxes vascular smooth muscle and reduces contractility. The net effect is decreased heart rate, decreased contractility, and coronary vasodilation, all lowering myocardial oxygen demand.

Lipid-lowering drugs

Anticoagulants and antiplatelets

The distinction the instructor draws: anticoagulants prevent clots from forming; antiplatelets prevent platelets from aggregating onto a clot that already exists.

Warfarin requires frequent INR monitoring, which is why many providers now favor apixaban or rivaroxaban. Glycoprotein IIb/IIIa inhibitors work by stopping fibrinogen from binding and forming bridges between platelets.

Beyond drugs

• Blood pressure control · smoking cessation · cardiac rehab
• Diet · exercise · diabetes management
• Depression management · patient education · flu vaccination

1.19 Sudden Cardiac Death

Abrupt, unexpected death resulting from a variety of cardiac causes. The posted exam study guide asks specifically about common causes.

A patient who survives SCD remains at risk of another event, because scarred myocardium creates ongoing electrical instability.

Interprofessional and nursing care after SCD

• Work the patient up to determine whether an MI caused the event.
• Cardiac catheterization, PCI, or CABG as indicated.
• Holter monitor — worn on the outside of the skin, typically for 24 hours, sometimes one to two weeks — or an implantable loop recorder.
• Electrophysiology study (EPS).
• Drug therapy.
• Teach family and caregivers CPR and AED use.
• Implantable cardioverter-defibrillator (ICD) — the most common approach to improving survival from SCD and preventing recurrence. Covered in full in Unit 2.

2.1 The Conduction System

Depolarization and repolarization

The heart cell membrane is semipermeable. At rest, the inside of the cell holds high potassium and low sodium, while the outside holds high sodium and low potassium, leaving the inside negatively charged. When cells are stimulated, permeability changes and sodium rushes in — depolarization. The slower movement of ions restoring the polarized state is repolarization.

The instructor flags that these words get used interchangeably with contraction and relaxation, which is exactly what makes EKG questions confusing. Fix the translation in your head first and every waveform description becomes readable.

The pathway and the intrinsic rates

Autonomic control

• Parasympathetic (vagus nerve) stimulation → slows SA node firing and slows AV node conduction → decreased heart rate. This is why vagal maneuvers work on SVT.
• Sympathetic stimulation → increases SA node firing, AV conduction, and contractility → increased heart rate. The instructor's example: a patient with a fever has a high heart rate for this reason.

2.2 Lead Placement

Five-lead — the telemetry monitor

Twelve-lead

Each lead views the heart from a different angle. A 12-lead can show structural changes, conduction changes, damage (infarction or ischemia), electrolyte imbalances, and drug toxicity.

2.3 Reading the Paper and Calculating Rate

Rate calculation

• The formal method: count QRS complexes in one full minute.
• The practical method: count the QRS complexes in a six-second strip and multiply by 10.
• Confirm a strip is six seconds by counting 30 large boxes — 30 × 0.20 sec = 6 seconds.

2.4 What Each Part of the EKG Represents

The posted exam study guide asks this by name: "What does each part of EKG represent in heart function?" It is asking for the mapping from waveform to mechanical event, not just the normal durations. Learn both columns.

2.5 ST Elevation and Contiguous Leads

• ST elevation must be at least 1 mm (one small box) above the isoelectric line.
• It must appear in 2 contiguous leads — two leads viewing adjoining regions of the heart.
• Exception: in V2 and V3 the elevation must be at least 2 mm.

2.6 A Systematic Approach to Any Strip

Use the same order every time. This is the method she demonstrated live on a strip, and it is what turns an unfamiliar rhythm into a set of answerable questions.

Measuring, practically

Count small boxes and multiply by 0.04. Her worked examples: a PR interval spanning 5 small boxes = 0.04 × 5 = 0.20 sec, normal. A QRS spanning 2 boxes = 0.08 sec, normal. A QT of about 11 boxes = 0.44 sec, roughly normal. For comparing intervals she suggests calipers, a ruler, or marking a sticky note against the strip and moving it complex to complex.

2.7 The Sinus Rhythms

In all three, everything is normal except the rate. The impulse still originates in the SA node, so a normal P wave precedes every QRS.

Symptomatic sinus bradycardia is treated with IV atropine. From Lewis Ch. 39, filling in a step the slide does not carry: if atropine is ineffective, the next steps are transcutaneous pacing or a dopamine or epinephrine infusion — the same escalation you will see again under the AV blocks.

2.8 Premature Atrial Contraction

A contraction starting from an ectopic focus in the atrium — somewhere other than the SA node — sooner than the next expected beat. Because the impulse does not start at the SA node, the P wave looks different.

Treatment in a healthy heart is aimed at the trigger — reduce caffeine, address tobacco use, treat thyroid disease. In a patient with heart disease you still address those triggers, but look further as well.

2.9 Paroxysmal Supraventricular Tachycardia

Also called supraventricular tachycardia or atrial tachycardia. A dysrhythmia starting in an ectopic focus anywhere above the bifurcation of the bundle of His.

Mechanism and associations

• Reentry phenomenon — re-excitation of the atria. The signal circles back on itself and re-fires the atria over and over. Usually a PAC triggers the run of repeated premature beats.
• Can occur with Wolff-Parkinson-White (WPW) syndrome or preexcitation through accessory conduction pathways.
• Causes: overexertion, emotional stress, deep inspiration, stimulants (caffeine, tobacco).
• Associated with rheumatic heart disease, digitalis toxicity, CAD, and cor pulmonale.

Sinus tachycardia vs SVT — the discrimination

Treatment ladder

2.10 Atrial Flutter

• Originates from a single ectopic focus, usually in the right atrium, less often the left.
• Associated with CAD, hypertension, mitral valve disorders, pulmonary embolus, chronic lung disease, cor pulmonale, cardiomyopathy, hyperthyroidism.
• Drugs that can cause it: digoxin, quinidine, epinephrine.

Treatment

• Goal: slow the ventricular response by increasing AV block.
• Calcium channel blockers, beta blockers.
• Synchronized cardioversion.
• Antidysrhythmics to convert to or maintain NSR: ibutilide (Corvert), amiodarone, flecainide.
• Radiofrequency catheter ablation is the treatment of choice for atrial flutter. Done in the electrophysiology lab; low-voltage, high-frequency energy destroys the ectopic focus through a catheter in the right atrium.

2.11 Atrial Fibrillation

Total disorganization of atrial electrical activity from multiple ectopic foci — as opposed to flutter's single focus. The result is loss of effective atrial contraction. The instructor's image: the heart is quivering rather than pumping, so blood stays stagnant instead of leaving the heart, and clots form.

• Paroxysmal — starts and stops spontaneously. Persistent — lasting more than seven days. Some patients are in chronic AF permanently.
• Prevalence increases with age.
• Usually occurs with underlying heart disease (CAD, valvular disease, cardiomyopathy).
• Can develop acutely with thyrotoxicosis, alcohol intoxication, caffeine, electrolyte problems, stress, or after heart surgery.
• Rapid ventricular response (RVR) — the ventricles contracting very fast in response to the chaotic atrial activity.
• Complications: decreased cardiac output, emboli, stroke.

2.12 Junctional Dysrhythmias

Named specifically on the posted exam study guide — the only individual rhythm singled out by name. Expect at least one question.

Treatment — only if symptomatic

• Rate too slow with symptoms (lightheaded, dizzy, syncope) → atropine.
• If caused by a drug, stop the offending agent — digoxin, nicotine, amphetamines, and caffeine can all cause it.
• Rate too fast → beta blockers, amiodarone, or calcium channel blockers.

2.13 The AV Blocks

Take these as an escalating series. Each one degrades conduction from atria to ventricles a little further, and the treatment escalates with it.

First-degree AV block

• Every impulse is conducted through the AV node, but AV conduction time is prolonged.
• Causes: increasing age, MI, CAD, rheumatic fever, hyperthyroidism, certain drugs, electrolyte imbalances.
• Usually not serious; the patient is asymptomatic. No specific treatment.

Second-degree, Type I (Mobitz I, Wenckebach)

• Causes: drugs (digoxin, beta blockers), CAD and other conditions that slow AV conduction.
• Clinical significance: usually due to myocardial ischemia or inferior MI. For most patients it is transient and well tolerated, but it can warn of a more serious block.
• Asymptomatic: monitor the rhythm and keep a transcutaneous pacemaker on standby.
• Symptomatic: atropine, or a temporary pacemaker.

Second-degree, Type II (Mobitz II)

• A P wave is non-conducted without progressive PR lengthening — this is the entire distinction from Mobitz I.
• More serious, because a set number of SA node impulses never reach the ventricles. Look for ratios like 2:1 or 3:1.
• Often progresses to third-degree (complete) heart block.
• Reduced heart rate → reduced cardiac output → hypotension and myocardial ischemia.
• Indication for a permanent pacemaker.
• Treatment: transcutaneous or temporary pacemaker may be needed before the permanent one is inserted if the patient is symptomatic.

Third-degree AV block (complete heart block)

AV dissociation — no impulses from the atria reach the ventricles. The atria and ventricles contract independently of each other, each to its own drummer. The escape pacemaker may sit above or below the bifurcation of the bundle of His.

• Associated with severe heart disease: CAD, MI, myocarditis, cardiomyopathy, and systemic diseases such as scleroderma.
• Drug causes: digoxin, beta blockers, calcium channel blockers.
• Significance: reduced cardiac output with ischemia, heart failure, and shock. Syncope from severe bradycardia or asystole.

2.14 Premature Ventricular Contraction

The contraction comes from an ectopic focus in the ventricles rather than the conduction system above them. Because it bypasses the normal fast pathway, the QRS is wide and bizarre.

• Causes: stimulants (caffeine, alcohol, nicotine, epinephrine), electrolyte imbalances, fever, hypoxia, exercise, emotional stress.
• Not usually harmful in a patient with a normal heart — many people feel them as palpitations.
• In CAD or acute MI, PVCs indicate ventricular irritability and may reduce cardiac output, leading to angina and heart failure.
• Treatment: treat the underlying cause. Drugs — beta blockers, lidocaine, amiodarone.

2.15 Ventricular Tachycardia

A run of three or more PVCs. The ectopic focus or foci fire repeatedly and the ventricle takes over as pacemaker. The instructor calls VT an ominous sign: it is life-threatening because of decreased cardiac output and the possibility of deteriorating into ventricular fibrillation.

Forms of VT

• Monomorphic — QRS complexes have the same shape, size, and direction.
• Polymorphic — QRS complexes change shape, size, and direction over a series of beats. Torsades de pointes is polymorphic VT with a prolonged QT.
• Sustained — more than 30 seconds. Nonsustained — less than 30 seconds.

• Associated with MI, CAD, significant electrolyte imbalances, cardiomyopathy, long QT syndrome, drug toxicity, CNS disorders. Can also occur with no evidence of heart disease.
• Severe decrease in cardiac output → hypotension, pulmonary edema, decreased cerebral blood flow, cardiopulmonary arrest.

2.16 Ventricular Fibrillation

Multiple ectopic foci fire in the ventricle at once. The ventricle simply quivers with no effective contraction, so there is no cardiac output. The patient is unresponsive, pulseless, and apneic. This is a lethal dysrhythmia — if it is not treated quickly the patient will not recover.

• Associated with acute MI, myocardial ischemia, heart failure, cardiomyopathy.
• Can occur during cardiac catheterization procedures — any manipulation of the conduction system.
• May occur after coronary reperfusion with thrombolytic therapy.
• Hyperkalemia and drug toxicity are also causes.

2.17 Asystole

• Total absence of electrical activity — essentially a flat line, though occasional P waves may be seen.
• The patient is unresponsive, apneic, and pulseless. Lethal, and needs immediate treatment.
• VF can masquerade as asystole — always check more than one lead before calling it.
• Results from advanced heart disease, a severe conduction system problem, or end-stage heart failure.
• Treatment: CPR and ACLS. Epinephrine 1 mg IV every 3–5 minutes. Intubation. Identify underlying causes.

2.18 Pulseless Electrical Activity

Organized electrical activity appears on the monitor — it may even look like normal sinus rhythm — but there is no mechanical heart activity and the patient has no pulse. Commonly seen after defibrillation.

Treatment: CPR, drug therapy, intubation, and correcting the reversible cause.

2.19 Treatment of Life-Threatening Dysrhythmias

Named as its own line on the posted exam study guide. The single most testable idea in this section is which rhythms get shocked and which do not.

Defibrillation

• Treatment for VF and pulseless VT.
• Rapid defibrillation within 2 minutes is critical to a successful outcome.
• Passes an electrical shock through the heart to depolarize the myocardial cells all at once. The goal is that after repolarization the SA node resumes as pacemaker.
• Biphasic — energy in two directions; lower energies, fewer post-shock dysrhythmias. First and successive shocks at 120–200 joules.
• Monophasic — energy in one direction; initial shock at 360 joules.
• Everyone must be clear before the shock. Resume chest compressions immediately after delivering it.
• An AED detects the rhythm and tells the user whether to shock, using hands-free pads.

Synchronized cardioversion

• Therapy of choice for ventricular tachydysrhythmias with a pulse and supraventricular tachydysrhythmias. The two examples printed on the cardioversion slide are VT with a pulse and atrial flutter with RVR; her PSVT and atrial fibrillation slides separately list cardioversion for the hemodynamically unstable patient.
• The synchronized circuit delivers the shock on the R wave of the QRS complex. The synchronizer switch must be turned on.
• Sedate the patient beforehand if it is not an emergency — IV sedation, and maintain the airway. If the patient becomes hemodynamically unstable, do it immediately without sedation.
• Initial energy: monophasic 100 joules; biphasic 50–100 joules. Increase as needed.
• If the patient becomes pulseless or converts to VF, turn the synchronizer switch OFF and defibrillate.

2.20 Implantable Cardioverter-Defibrillator

The posted exam study guide pairs pacemakers and ICDs and asks specifically for patient education and teaching.

• The lead system is placed through the subclavian vein to the endocardium.
• The battery-powered pulse generator is implanted over the pectoral muscle on the patient's non-dominant side — so they use that arm less.
• It monitors rate and rhythm, identifies VT and VF, and delivers a 25-joule shock. More shocks follow if the first is unsuccessful.

ICD patient teaching

• Follow up with the provider for routine ICD function checks.
• Watch for signs of infection at the site — redness, swelling, drainage.
• Do not lift the arm on the ICD side until cleared by the provider.
• Avoid large magnets and strong electromagnetic fields — they interfere with the device.
• No MRI unless the ICD is approved as MRI-safe or a safety protocol is in place.
• Do not stand near antitheft devices in store doorways — walk through at a normal pace.
• Carry the ICD card at all times.
• Anxiety is common. Encourage ICD support groups.

2.21 Pacemakers

An electronic device that paces the heart when the normal conduction pathway is damaged. The electrical stimulus travels from the pulse generator through the leads to the myocardial wall; the muscle is captured and stimulated to contract.

Demand pacemakers are the most common. They sense the heart's own electrical activity and fire only when the rate falls below a preset threshold. Two features: a sensing device that inhibits pacing when the rate is adequate, and a pacing device that triggers when no QRS occurs within a preset time.

Temporary pacemakers

Permanent pacemakers and CRT

• Totally implanted. Power source placed subcutaneously over the pectoral muscle on the non-dominant side; pacing leads placed transvenously to the right atrium and/or one or both ventricles.
• Cardiac resynchronization therapy (CRT) — also called biventricular pacing. Resynchronizes the cardiac cycle by pacing both ventricles, improving ventricular function. Used in patients with heart failure.
• Antitachycardia pacing — a stimulus delivered to the ventricle to terminate a tachydysrhythmia such as VT.
• Overdrive pacing — pacing the atrium at 200–500 impulses per minute to stop an atrial tachycardia such as atrial flutter with RVR.

Pacemaker malfunction

Start from what should happen: after an atrial pacer fires you should see a P wave; after a ventricular pacer fires you should see a QRS. Two things can go wrong.

Indications for a permanent pacemaker

• Acquired AV block · second-degree AV block · third-degree AV block
• Atrial fibrillation with a slow ventricular response
• Bundle branch block
• Cardiomyopathy — dilated and hypertrophic
• Heart failure · SA node dysfunction
• Symptomatic bradycardia of unknown cause
• Tachydysrhythmias such as ventricular tachycardia — though the instructor notes these patients are usually better served by an ICD, since it can shock

Pacemaker nursing management and teaching

• Before transcutaneous pacing, explain that the muscle contractions produced as current passes through the chest wall are uncomfortable. Provide analgesia or sedation when possible.
• Monitor the EKG.
• After permanent placement the patient will be in a sling — teach them not to lift that arm above shoulder level, so the leads are not displaced.
• Check the insertion site for infection and bleeding.
• Assess for hiccups.

2.22 Master Rhythm Reference

All fourteen rhythms in one place, in the order she taught them. Use this for final review; use the individual sections above to understand why each row reads the way it does.

3.1 The Reasoning Tool — Follow the Blood

There are eight valve lesions in this unit and memorizing eight symptom lists is the wrong strategy. The instructor teaches a method instead, and returns to this figure before every single lesion: locate the valve, name what it does, then ask what backs up when it fails. The manifestations follow from the anatomy.

Stenosis versus regurgitation

3.2 Rheumatic Fever and Rheumatic Heart Disease

What it is

• Rheumatic fever (RF) is an acute inflammatory disease that can involve all layers of the heart.
• Rheumatic heart disease (RHD) is the chronic scarring and deformity of the heart valves resulting from RF.
• RF occurs as a complication 2–3 weeks after group A streptococcal pharyngitis. RHD results from valve damage caused by an abnormal immune response to Streptococcus.
• RF affects the heart, skin, joints, and CNS. RHD mainly affects children and young adults.
• About 50% of RF episodes are rheumatic pancarditis — endocardium, myocardium, and pericardium all involved.

What it does to the valves

Rheumatic infective endocarditis attacks the valves: swelling and erosion of the leaflets, vegetation forming from fibrin and blood cell deposits, thickened leaflets, fusion of the commissures and chordae tendineae, and fibrosis of the papillary muscle. Calcified leaflets produce stenosis; leaflets too stiff to close produce regurgitation. The mitral and aortic valves are most often affected — which is exactly why rheumatic disease turns up as the leading cause of mitral stenosis later in this unit.

Aschoff's bodies are nodules formed by the inflammatory reaction, with swelling and destruction of collagen fibers. As they age they become fibrous and leave scar tissue in the myocardium. Damage begins during the first attack; recurrent infections cause further structural damage.

Jones criteria

Carditis produces three signs: murmurs of mitral or aortic regurgitation or mitral stenosis; heart enlargement and heart failure from myocarditis; and pericarditis with muffled heart sounds, chest pain, friction rub, or effusion. Arthritis affects the larger joints — knees, ankles, elbows, wrists — with swelling, heat, redness, tenderness, and limited motion.

Diagnosis and treatment

• No single diagnostic test exists for RF.
• The most consistent ECG change is a prolonged PR interval, from delayed AV conduction.
• Echocardiogram may show valvular insufficiency and pericardial fluid or thickening. Chest x-ray may show an enlarged heart.
• Treatment: antibiotics, salicylates, NSAIDs, and corticosteroids for fever and joint manifestations; bed rest or limited activity to reduce cardiac workload.
• Antibiotics do not change the course of the acute disease or prevent carditis — they eliminate residual streptococci in the tonsils and pharynx and prevent spread to others.

Prevention — the line the instructor emphasizes

3.3 Mitral Valve Stenosis

Where: between the left atrium and left ventricle. Job: when left atrial pressure rises, the mitral valve opens to let blood into the left ventricle, then closes so the ventricle can contract without backflow.

• Most common cause: rheumatic heart disease — from untreated strep. Other causes: age, congenital.
• Rheumatic infective endocarditis scars the valve leaflets and chordae tendineae, narrowing the two mitral leaflets.

Clinical manifestations

• Exertional dyspnea — reduced lung compliance
• Loud, accentuated S1 (first heart sound)
• Low-pitched diastolic murmur, best heard at the apex
• Chest pain — from decreased cardiac output and coronary perfusion
• Atrial fibrillation, emboli, stroke
• The textbook adds: hoarseness (left atrial pressure on the laryngeal nerve), hemoptysis (from pulmonary hypertension), fatigue, palpitations

3.4 Mitral Valve Regurgitation

The mitral valve fails to close completely, so during ventricular systole blood flows backward into the left atrium instead of forward through the aorta. From the left atrium it backs into the lungs — pulmonary hypertension and pulmonary congestion.

• Primary MR — a problem with the leaflets themselves.
• Secondary MR — due to myocardial disease (MI, rheumatic heart disease).
• Most cases are caused by MI, chronic rheumatic heart disease, mitral valve prolapse, or ischemic papillary muscle dysfunction.

Clinical manifestations

• Chronic MR is asymptomatic for years.
• When symptomatic, the picture is left ventricular failure: weakness, fatigue, dyspnea, orthopnea, paroxysmal nocturnal dyspnea, peripheral edema.
• S3 — the third heart sound, also called a ventricular gallop.
• Loud, holosystolic murmur heard at the apex, radiating to the left axilla.
• Acute MR is poorly tolerated — a new systolic murmur with pulmonary edema, and cardiogenic shock develops rapidly.

3.5 Mitral Valve Prolapse

• An abnormality of the mitral leaflets and papillary muscles of the chordae that allows the leaflets to prolapse into the left atrium during systole.
• Usually benign and usually asymptomatic, but can lead to mitral regurgitation and eventually heart failure.
• Cause unknown; there may be a genetic link.
• Can occur in connective tissue disorders such as Marfan syndrome.
• Manifestations when present: palpitations, dyspnea, chest pain, activity intolerance, syncope, holosystolic murmur.

3.6 Aortic Valve Stenosis

Where: between the left ventricle and the aorta. Job: opens during systole to let the left ventricle eject blood to the entire body. Stenosis obstructs that outflow, so cardiac output falls — and everything downstream suffers.

• Congenital AS is found in childhood, adolescence, or young adulthood.
• In older adults it can result from rheumatic fever; the valve leaflets harden and stiffen. Note the textbook nuance: AS affects 3% of people over 65, and in that group it is usually non-rheumatic — degenerative calcification.

• Crescendo-decrescendo, holosystolic murmur that may radiate to the carotids — her slide's exact wording.
• Slow, weak carotid pulse — the downstream consequence of reduced cardiac output.

3.7 Aortic Valve Regurgitation

The aortic valve fails to close completely, so blood flows backward from the aorta into the left ventricle during diastole.

• Caused by primary disease of the aortic root, the valve leaflets, or both.
• Acute causes — an emergency: aortic dissection, infective endocarditis, trauma.
• Chronic causes: rheumatic heart disease, congenital bicuspid aortic valve, syphilis, connective tissue problems, post-surgical.

Clinical manifestations

• Some patients develop sudden cardiovascular collapse: severe dyspnea, chest pain, and hypotension — indicating cardiogenic shock, a life-threatening emergency.
• Chronic AR can be asymptomatic.
• Chronic, severe AR: water-hammer pulse — a strong, quick beat that collapses immediately.
• Heart sounds: soft or absent S1, plus S3 or S4, and a soft, high-pitched diastolic murmur.
• The textbook adds for chronic AR: fatigue, exertional dyspnea, orthopnea, PND, heaving precordial impulse.

3.8 The Right-Sided Valves

Apply the same method. The tricuspid and pulmonic valves sit on the right side, so when they fail, blood backs up into the body rather than the lungs — and the picture is right-sided heart failure.

Tricuspid regurgitation

• Primary TR — less common. Caused by chest trauma, tumors, infective endocarditis, rheumatic fever, or congenital malformation.
• Secondary TR — right ventricular and right atrial dilatation from pulmonary hypertension, cor pulmonale, or pulmonary outflow tract obstruction.
• Backflow into the right atrium during systole.
• Usually no symptoms until severe. When they appear, they are the signs of right-sided heart failure: fatigue, shortness of breath, hepatomegaly, peripheral edema, jugular vein distention.

Tricuspid stenosis

• Usually caused by rheumatic fever. Restricts flow from right atrium to right ventricle.
• Fluttering discomfort in the neck, fatigue.
• Peripheral edema, ascites, hepatomegaly.
• Diastolic, low-pitched murmur with increased intensity during inspiration.

Pulmonic regurgitation

• The pulmonic valve fails to close, so blood flows back into the right ventricle, which dilates.
• Causes: pulmonary hypertension, surgical repair of tetralogy of Fallot, congenital valve disease.
• Usually asymptomatic. Crescendo-decrescendo murmur.

Pulmonic stenosis

• A stenotic pulmonic valve makes it hard for blood to reach the lungs. Caused by congenital heart disease.
• Results in right ventricular hypertension and hypertrophy.
• Usually asymptomatic. If symptomatic, the picture resembles aortic stenosis: syncope, dyspnea, angina.

3.9 All Eight Lesions at a Glance

3.10 Diagnostic Studies

The posted exam study guide asks for diagnostic tests by name.

3.11 Treatment

1. Conservative therapy

Many valve disorders are asymptomatic. When symptoms arrive they come as heart failure, acute pulmonary edema, or thromboembolism, and the goal is to prevent exacerbation.

• Heart failure: vasodilators and positive inotropes (drugs that increase the strength of cardiac contraction, so the heart moves more blood with fewer beats), beta blockers, diuretics, low-sodium diet.
• Atrial dysrhythmias: calcium channel blockers, beta blockers, antidysrhythmic drugs, or electrical cardioversion.
• Anticoagulants in patients with atrial fibrillation, to prevent emboli.
• Prevent infective endocarditis.

2. Percutaneous transluminal balloon valvuloplasty (PTBV)

• Done in the cath lab, similar in approach to PCI.
• A balloon-tipped catheter is threaded through the femoral vein or artery to the stenotic valve and inflated to separate the leaflets.
• Not a permanent fix.
• Treats mitral, tricuspid, pulmonic, and aortic stenosis — the stenotic lesions, since the problem is an opening that will not open.

3. Surgical therapy — repair vs replacement

• Valve repair is preferred, because it carries a lower operative mortality rate. Used for mitral and tricuspid valve disease.
• Open surgical valvuloplasty — suturing torn leaflets, chordae tendineae, or papillary muscles.
• Annuloplasty — reconstruction of the annulus, the ring around the valve, with or without prosthetic rings.
• Valve replacement may be needed for mitral, aortic, tricuspid, and pulmonic disease.

Mechanical versus biological valves

3.12 Transcatheter Aortic Valve Replacement

Called out by name on the posted exam study guide — "TAVR: nursing care / what is it."

• For patients with severe, symptomatic aortic stenosis.
• A minimally invasive alternative to open-heart surgery.
• Planning beforehand: coronary CT angiogram, echocardiogram, or cardiac catheterization.
• Transfemoral approach — a catheter delivers the new valve to the site and a balloon is inflated to seat it.
• Three valves currently available: Edwards Sapien 3, CoreValve transcatheter aortic valve, and the Lotus valve.

Nursing care after TAVR

• Monitor vital signs.
• Assess for bleeding at the femoral site — this is the access point.
• Assess for infection; monitor and assess the incision site.
• Pain management.
• Early ambulation and deep breathing exercises — incentive spirometry.
• Cardiac monitoring for dysrhythmias — the patient will likely be on continuous EKG in the ICU.
• Psychological support for the patient and family.

3.13 Nursing Management of Valvular Disorders

• Encourage early intervention and treatment of strep throat to prevent rheumatic fever and RHD.
• Teach patients with a history of rheumatic fever or infective endocarditis to report signs of valvular heart disease.
• Design activities to match the patient's needs — an exercise program can increase cardiac tolerance.
• Teach the patient to limit activities that cause fatigue and dyspnea, and to avoid strenuous activity, because damaged valves cannot handle the increased cardiac output.
• Discourage tobacco use; provide cessation resources when the patient is ready.
• Refer to a counselor if the patient has a stressful job.
• Perform cardiac assessments — EKGs and heart sounds — to evaluate drug effectiveness.
• Teach the side effects of medications. Her reasoning: a patient who knows a side effect is expected is more likely to stay on the drug rather than stopping it abruptly when something uncomfortable happens.
• After valve surgery on warfarin, monitor the INR — 2.5 to 3.5 for a mechanical valve.

Where it comes from

This is the assigned reading, worked through before any of the instructor's slides or lecture material existed — Lewis’s Medical-Surgical Nursing, 12th ed., Ch. 37 (pp. 819–859), Ch. 39 (pp. 884–909) and Ch. 40 (pp. 909–925), plus the posted unit objectives.

Nothing here is attributed to the instructor, because none of it came from her. The boxes marked HIGH-YIELD are the textbook’s emphasis and this guide’s, which is why they are a different colour from the yellow instructor boxes in Study. There are no lecture play buttons in this view for the same reason.

1.2 The atherosclerotic process

• Starts with endothelial injury — tobacco, hyperlipidemia, hypertension, toxins, diabetes, inflammation, infection damage the intima.
• Intima = innermost arterial layer. Normally nonreactive to platelets and leukocytes; injury changes that.
• Inflammation is central — CRP is a nonspecific liver-made marker of systemic inflammation, often elevated in CAD.
• Lipoprotein(a) and homocysteine damage vessel lining, promote plaque, and make clots more likely. Not part of routine risk screening — reserved for intermediate/high-risk patients.

1.3 Risk factors

• Age/gender: risk rises for men >45 and women >55. Women are diagnosed about 10 years later than men (possible estrogen effect); HRT does not protect and may harm.
• Women present atypically — fatigue is often the first ACS symptom; also dyspnea, upper back pain, indigestion, memory problems, palpitations, anxiety. More silent MIs, more first-event UA than MI.
• Diabetes: CAD incidence is 2-4x greater even with good glucose control; target A1C <7%. Silent ischemia is common (autonomic neuropathy).
• Tobacco: nicotine → catecholamine release → ↑HR, vasoconstriction, ↑BP. Carbon monoxide occupies hemoglobin sites and injures endothelium. Secondhand smoke raises risk 25-30%.
• Family history under age 55 is “premature CAD” and carries extra weight.

1.5a Prevention and lipid management

• Physical activity — FITT: Frequency, Intensity, Type (isotonic), Time. Goal 150 min/wk moderate (30 min × 5 days) or 75 min/wk vigorous.
• Post-MI intensity rule: if no exercise stress test has been done, HR should not exceed 20 beats/min over resting HR.
• Diet: fat 25-35% of calories, saturated fat <7%, cholesterol <200 mg. Omega-3s lower triglycerides but do not affect LDL.
• Statins (HMG-CoA reductase inhibitors) are first-line; adverse effects are rare but include liver damage and myalgia progressing to rhabdomyolysis. Monitor liver enzymes; check CK if muscle aches.
• Niacin: flushing within 20 min lasting 30-60 min — premedicate with aspirin 30 min before.
• Bile-acid sequestrants block absorption of other drugs — give others 1 hr before or 3-4 hr after.
• Aspirin for primary prevention is controversial — may be used ages 40-59 at higher CAD risk without bleeding risk; should not be started for primary prevention after age 60.

Covers: Lewis Ch. 37, p. 819-830

CAD is atherosclerosis of the coronary arteries. Everything else in this week — angina, ACS, most dysrhythmias, sudden cardiac death — grows out of this one process. Know the three developmental stages and which risk factors are modifiable.

1.5b The A-B-C-D-E-F treatment mnemonic

1.7a Types of angina

1.7b Precipitating factors to teach

• Circadian rhythm — symptoms cluster in early morning and the first hours after waking.
• Heavy meal — blood diverts to GI tract. Teach rest 1-2 hr after a heavy meal.
• Physical exertion — ↑HR shortens diastole, which is when coronary filling occurs. Isometric arm work (raking, shoveling snow, lifting) is a classic trigger.
• Temperature extremes, strong emotions, sexual activity, stimulants (cocaine, amphetamines), tobacco.

1.18 Drug therapy

Covers: Lewis Ch. 37, p. 830-837

Angina is the clinical manifestation of myocardial ischemia — demand exceeds supply. Ischemia is reversible; infarction is not. The whole drug strategy is either lower O₂ demand or raise O₂ supply.

• Ischemia typically requires 70% stenosis of a coronary artery (or 50% for the left main).
• Chronic stable angina = intermittent chest pain over a long period with a similar pattern of onset, duration, and intensity. Provoked by exertion, stress, or emotional upset.
• Usually lasts only a few minutes and subsides when the precipitating factor is resolved (rest, calming down, SL NTG). Pain at rest is unusual and suggests UA.
• Chronic angina pain usually does not change with position or breathing — a key differentiator from pericarditis.
• ECG in ischemia: ST depression and/or T wave inversion. ST depression is significant at ≥1 mm below isoelectric in ≥2 contiguous leads. Changes return to baseline when flow is restored.

1.6 Sorting the three syndromes

• ST elevation is significant at ≥1 mm above isoelectric in ≥2 contiguous leads (leads viewing the same wall) — except V2 and V3, which require ≥2 mm.

• Pathologic Q wave = deep, or ≥1/3 the height of the R wave in the same lead. It appears within 1-2 days if reperfusion is delayed, and remains on the ECG forever. With early reperfusion, Q waves may never develop.
• Serial 12-lead ECGs are done because MI is a dynamic process; always compare to a previous ECG when possible.

1.11 Serum cardiac biomarkers

1.13 Localizing the infarct

Covers: Lewis Ch. 37, p. 840-846

ACS is what happens when a stable plaque ruptures. Partial occlusion produces UA or NSTEMI; total occlusion produces STEMI. Two data points sort all three: the ST segment and the troponin.

Healing and remodeling

Beyond the lecture guide — Post-MI healing and remodeling timeline; not lectured.

Complications of MI

Beyond the lecture guide — Complications of MI; not covered in the lecture.

1.5c Rehabilitation, activity, and teaching

• 1 MET = O₂ needed at rest = 3.5 mL O₂/kg/min.
• By discharge the patient should tolerate 3-6 METs.
• Isometric activity (lifting, carrying, pushing) triggers Valsalva and changes HR/BP rapidly — limit it. Isotonic activity (walking, swimming, cycling) puts a safe steady load on the heart.
• Teach patients to stop and rest for chest pain or shortness of breath, and that HR should return to resting within a few minutes of stopping. Symptoms matter more than an absolute target HR — many patients are on β-blockers and cannot reach a target rate.
• Sexual activity is a moderate-energy activity, roughly climbing 2 flights of stairs or walking briskly. Generally safe when the patient can achieve 3-5 METs without chest pain or excessive dyspnea. Wait 3-4 hr after a large meal; avoid extremes of temperature; avoid anal intercourse (vasovagal response); erectile dysfunction drugs within 48 hr are contraindicated with any nitrate.
• Screen for depression — common after CAD, especially in women, and linked to poor exercise adherence.

1.14 Percutaneous coronary intervention

• Balloon angioplasty compresses plaque against the artery wall; an intracoronary stent is usually placed after.
• Bare metal stent (BMS) vs drug-eluting stent (DES) — DES is coated with a drug to reduce neointimal hyperplasia. In-stent restenosis (ISR) is scar tissue building inside the stent, months to a year later; risk is lower with DES.
• Stents are thrombogenic, so dual antiplatelet therapy (DAPT) is required until the intimal lining covers the metal.

• PCI complications: abrupt closure from dissection/rupture, vascular injury at the access site, acute MI from stent thrombosis or distal plaque embolization, stent embolization, failure to cross the lesion, coronary spasm, dye allergy, renal problems, bleeding (including retroperitoneal bleeding with femoral access), infection, stroke, need for emergent CABG.
• PCI may not be feasible with 3-vessel CAD or significant left main disease.

1.15 Thrombolytic (fibrinolytic) therapy

• Agents: reteplase, alteplase, tenecteplase — all IV. They lyse the fibrin meshwork.
• Only for STEMI, and only where PCI is unavailable or too far away. Never for UA or NSTEMI.
• Inclusion criteria: chest pain <12 hr with STEMI ECG findings, and no absolute contraindications. Pain of 12-24 hr may still be considered.
• Before starting: draw baseline labs, place 2 or 3 IV lines, and complete all other invasive procedures first to reduce bleeding risk.
• Signs of reperfusion: the most reliable is return of the ST segment to baseline. Others: resolution of chest pain, and an early rapid rise in biomarkers as necrotic cells wash out. Reperfusion dysrhythmias (accelerated idioventricular rhythm) are a less reliable sign and are usually self-limiting.
• IV heparin is started afterward because reocclusion is a major concern.
• Minor bleeding (IV sites, gums) is expected — control with manual pressure, pressure dressing, or ice.

1.16 CABG surgery

• Indicated for failure of medical management, left main or 3-vessel disease, poor PCI candidacy, or continued pain after PCI.
• Left internal mammary artery (LIMA) is the most common graft — proximal end stays attached to the left subclavian; distal end is sutured beyond the blockage, usually to the LAD. IMAs have longer patency than saphenous veins.
• Saphenous vein grafts are more prone to intimal hyperplasia, stenosis, and occlusion. Radial artery grafts are prone to spasm — treat with perioperative CCBs and long-acting nitrates, and monitor sensory/motor function of the hand.
• Cardiopulmonary bypass complications: systemic inflammation, bleeding and anemia from RBC/platelet damage, fluid and electrolyte imbalance, infection, hypothermia, neurologic and renal problems, dysrhythmias.
• Postoperative atrial fibrillation occurs in 20-50% of CABG patients. β-blockers are started at least 24 hr before surgery and restarted as soon as possible after to reduce incidence.
• Postoperative cognitive dysfunction (POCD) — impaired memory, concentration, language comprehension, social integration; usually improves within months.
• Grafts are subject to the same atherosclerotic process — CABG and PCI are palliative, not curative.

1.17 Priority drug therapy in ACS

• Aspirin 162-325 mg chewable as soon as ACS is suspected, unless truly allergic.
• IV nitroglycerin — immediate onset; titrate to eliminate chest pain; monitor BP closely. A hypotensive patient may be volume depleted and benefit from a fluid bolus — then assess for overload (crackles).
• Morphine — drug of choice for pain unrelieved by NTG. Vasodilates, lowers preload, contractility, BP, HR, and myocardial O₂ consumption; reduces anxiety. Monitor for bradypnea and hypotension.
• High-dose statin (atorvastatin 80 mg) in the ED.
• Oral β-blockers within 24 hr unless HF, heart block, or hypotension.
• ACE inhibitors within 24 hr if BP stable — limits remodeling; continued indefinitely for EF ≤40% or HF.
• Aldosterone antagonists (spironolactone, eplerenone) decrease mortality after STEMI unless hyperkalemia or elevated creatinine.
• Stool softeners — straining triggers the Valsalva maneuver, and vagal stimulation produces bradycardia and can provoke dysrhythmias.
• Anticoagulation (LMWH or UH) is used for UA and NSTEMI; STEMI patients go straight to cath.

Covers: Lewis Ch. 37, p. 837-840, 846-855

For STEMI, time is muscle. Everything in this unit is organized around one question: how fast can the artery be opened, and what does the nurse watch for afterward.

2.1a Conduction and the four properties of cardiac cells

• Normal pathway: SA node → atrial myocardium (interatrial and internodal pathways) → AV node → bundle of His → right and left bundle branches → Purkinje fibers.
• Vagal (parasympathetic) stimulation slows SA node firing and AV conduction → ↓HR. Sympathetic stimulation increases SA firing, AV conduction, and contractility → ↑HR.
• Depolarization = sodium rushes in, inside becomes positive. Repolarization = slower ion movement restores the polarized state.

2.1b Why dysrhythmias happen

• Mechanisms: disorders of impulse formation, impulse conduction, or both.
• Escape: if the SA node fires more slowly than a secondary pacemaker, the secondary site takes over at its intrinsic rate. Escape rhythms are a safety mechanism and should not be suppressed.
• Triggered/ectopic: a focus fires more rapidly than the SA node.
• Reentry: unidirectional block lets an impulse re-enter recovered tissue, causing a premature beat or rapid rhythm.
• Refractory periods: absolute (excitability is zero, cannot be stimulated) then relative (excitability returns) — the relative refractory period is why R-on-T is dangerous.
• Common causes: ischemia/MI, HF, valve disease, cardiomyopathy, conduction defects, accessory pathways, acid-base imbalance, electrolyte imbalances (hyperkalemia, hypocalcemia), hypoxia, drugs and drug toxicity, caffeine/tobacco/alcohol, sepsis and shock, thyroid problems, electric shock, emotional crisis.

2.2 Monitoring practicalities

• Most common continuous monitoring leads are II and V1. MCL1 (similar to V1) is used when only 3 leads are available.

• Skin prep: clip excess hair with scissors, rub gently with dry gauze until slightly pink, wipe oily skin with alcohol first, and apply a skin protectant if the patient is diaphoretic.
• Artifact is baseline/waveform distortion from loose leads, dried conductive gel, muscle activity (shivering, ambulating), or electrical interference. Fix the equipment before interpreting the rhythm.
• Telemetry is observation at a site distant from the patient — either a centralized continuously watched system or a detection-and-storage system with advanced alarms.

2.3 Reading the paper

• Horizontally, 1 small square = 0.04 sec; 1 large square (5 small) = 0.20 sec; 300 large squares = 1 minute.
• Vertically, 1 small square = 0.1 mV; 1 large square = 0.5 mV.
• 6-second method: count QRS complexes in 6 seconds (between the 3-second markers) × 10. Works for irregular rhythms.
• 1500 method: small squares between one R-R interval divided into 1500.
• 300 method: large squares between one R-R interval divided into 300.

• The last two are accurate only when the rhythm is regular. The most accurate method of all is counting QRS complexes over a full minute.

• ST changes (elevation, depression) → think ischemia, injury, infarction.
• T wave changes (tall peaked, inverted) → think electrolyte imbalance, ischemia, infarction.
• QT changes → think drugs, electrolyte imbalances, and heart rate. QT shortens as HR increases; a corrected QT (QTc) accounts for rate. Normal adult women have slightly longer QT intervals than men.

Covers: Lewis Ch. 39, p. 884-890

You cannot recognize a dysrhythmia without a system. Learn the paper, the waveforms, the normal intervals, and one consistent 10-step approach — then every rhythm becomes a comparison to normal.

2.7 Sinus rhythms

• Sinus bradycardia can be normal in aerobically trained athletes and during sleep. Also caused by Valsalva, hypothermia, increased intraocular pressure, vagal stimulation, β-blockers, and CCBs. Disease associations: hypothyroidism, increased intracranial pressure, and inferior MI.
• Symptomatic bradycardia = rate <60 plus symptoms of inadequate perfusion: pale cool skin, hypotension, weakness, angina, dizziness, confusion, shortness of breath, syncope.
• Treatment sequence for symptomatic bradycardia: IV atropine → if ineffective, transcutaneous pacing or a dopamine or epinephrine infusion → possibly a permanent pacemaker. If drugs caused it, they may be held, stopped, or reduced.
• Sinus tachycardia causes: exercise, fever, pain, hypotension, hypovolemia, anemia, hypoxia, hypoglycemia, ischemia, HF, hyperthyroidism, anxiety, fear; drugs including epinephrine, norepinephrine, atropine, caffeine, theophylline, hydralazine, and OTC pseudoephedrine.
• Tachycardia increases myocardial O₂ consumption — in CAD or acute MI it can cause angina or extend infarct size. Stable patients: vagal maneuvers, IV β-blockers, adenosine, or CCBs. Unstable patients: synchronized cardioversion.

2.8 Atrial dysrhythmias

2.12 Junctional dysrhythmias

• Arise in the AV junction when the SA node fails to fire or the signal is blocked; the AV node becomes the pacemaker.
• Impulse travels retrograde through the atria → inverted P wave just before or after the QRS, or hidden inside it. If the P precedes the QRS, the PR is <0.12 sec. QRS is usually normal.
• Junctional escape rhythm 40-60 · Accelerated junctional 61-100 · Junctional tachycardia 101-180.
• Escape rhythms are a safety mechanism and should not be suppressed. Accelerated junctional reflects sympathetic stimulation to improve CO. Junctional tachycardia signals a more serious problem and can reduce CO.
• Treatment: atropine for symptomatic escape rhythm; stop the offending drug if toxicity is the cause; β-blockers, CCBs, or amiodarone for rate control in the absence of digitalis toxicity.

Covers: Lewis Ch. 39, p. 890-896

Everything above the ventricles produces a narrow QRS, because once the impulse reaches the AV node it travels the normal pathway. What changes is the P wave and the regularity.

2.13 Third-degree AV block (complete heart block)

• No atrial impulses reach the ventricles. Atria and ventricles are stimulated and contract independently — AV dissociation.
• Atrial rate usually 60-100; ventricular rate depends on the escape site: 40-60 if in the AV node, 20-40 if in the His-Purkinje system. Both rhythms are regular but unrelated.
• QRS is normal if the escape rhythm starts at or above the bundle of His; widened if below it.
• Associated with severe heart disease: CAD, MI, myocarditis, cardiomyopathy, scleroderma; and drugs — digoxin, β-blockers, CCBs.
• Usually causes reduced CO with ischemia, HF, and shock. Syncope may result from severe bradycardia or periods of asystole.
• Treatment: transcutaneous pacing until a temporary transvenous pacemaker can be inserted, with dopamine or epinephrine as interim measures to raise HR and support BP. A permanent pacemaker is needed as soon as possible.

Covers: Lewis Ch. 39, p. 895-897

AV blocks are graded by how badly the signal gets from atria to ventricles: delayed, intermittently dropped, or completely disconnected. Work the PR interval first — it sorts three of the four.

• More serious — it often progresses to third-degree block and carries a poor prognosis. Reduced HR → decreased CO → hypotension and myocardial ischemia.
• Type II AV block is an indication for a permanent pacemaker. Transcutaneous or temporary transvenous pacing may bridge to it if the patient is symptomatic.

2.14 Premature ventricular contractions

• A PVC is an early QRS from a ventricular ectopic focus — wide and distorted, >0.12 sec, with the T wave usually opposite in direction to the QRS. P wave is rarely visible; PR is not measurable.
• Unifocal = same shape (one focus). Multifocal = different shapes (multiple foci).

• Bigeminy = every other beat is a PVC. Trigeminy = every third beat. Couplet = two consecutive PVCs. Three or more in a row = ventricular tachycardia.
• R-on-T phenomenon — a PVC landing on the T wave of the preceding beat, during the relative refractory period, when excitability is heightened. High risk of triggering VT or VF.
• Associated with caffeine, alcohol, nicotine, aminophylline, epinephrine, isoproterenol; electrolyte imbalances, hypoxia, fever, exercise, emotional stress; MI, mitral valve prolapse, HF, cardiomyopathy, CAD.
• PVCs are usually not harmful in a normal heart, but in CAD or acute MI they indicate ventricular irritability.
• Assess the patient, not just the strip: take an apical-radial pulse and determine the pulse deficit, because PVCs often do not generate a peripheral pulse.
• Treatment targets the cause (O₂ for hypoxia, electrolyte replacement). Drugs if needed: β-blockers, lidocaine, amiodarone. Isolated PVCs are usually not treated.

2.15 Ventricular tachycardia

• Three or more consecutive PVCs. Rate 150-250, regular or irregular, wide distorted QRS >0.12 sec, PR not measurable. AV dissociation may be present.
• Monomorphic = QRS complexes identical in shape, size, direction. Polymorphic = shape changes across beats. Torsades de pointes = polymorphic VT associated with a prolonged QT interval.
• Sustained = longer than 30 seconds; nonsustained = less than 30 seconds.
• Sustained VT severely drops CO — decreased diastolic filling time plus loss of atrial contraction → hypotension, pulmonary edema, decreased cerebral flow, cardiopulmonary arrest.
• VT must be treated quickly even if brief and self-terminating.

2.16 Ventricular fibrillation

• Irregular waveforms of varying shape and amplitude — multiple ectopic ventricular foci firing. The ventricle is quivering with no effective contraction, so there is no cardiac output.
• Rate not measurable; rhythm chaotic; no P waves; PR and QRS not measurable.

• The patient is unresponsive, pulseless, and apneic. VF is lethal.
• Occurs in acute MI, myocardial ischemia, HF, cardiomyopathy; during pacing or cath from catheter stimulation; with coronary reperfusion; and from electric shock, hyperkalemia, hypoxemia, acidosis, and drug toxicity.
• Treatment: immediate CPR and ACLS with defibrillation and drug therapy (epinephrine, amiodarone). There should be no delay in starting compressions or using a defibrillator once available.

2.17 Asystole and pulseless electrical activity

• Asystole — total absence of ventricular electrical activity; occasional P waves may be seen. Patient is unresponsive, pulseless, apneic. Usually reflects advanced heart disease, a severe conduction problem, or end-stage HF. Prognosis is very poor.
• VF may masquerade as asystole — always assess the rhythm in more than one lead.
• Treatment: CPR with ACLS, epinephrine, intubation, and efforts to determine the underlying cause. Asystole is not a shockable rhythm.
• PEA — organized electrical activity on the monitor with no mechanical activity and no pulse. It is the most common dysrhythmia seen after defibrillation.
• PEA prognosis depends entirely on finding and fixing the cause: hypovolemia, hypoxia, metabolic acidosis, hyperkalemia, hypokalemia, hypoglycemia, hypothermia, toxins/overdose, cardiac tamponade, thrombosis (MI or PE), tension pneumothorax, trauma.
• Treatment: CPR first, then drug therapy (epinephrine) and intubation, while correcting the cause.

Covers: Lewis Ch. 39, p. 897-899

Ventricular rhythms bypass the normal conduction pathway, so the QRS is wide and distorted. Two of the rhythms here are lethal, and one of them requires you to check a pulse before deciding what to do.

Accelerated idioventricular rhythm

Beyond the lecture guide — Instructor said this rhythm is not on the exam.

• Rate 40-100, regular, wide QRS, no visible P waves — a ventricular pacemaker outpacing a slower intrinsic pacemaker.
• Most often associated with acute MI and reperfusion after thrombolytics or PCI; also digitalis toxicity.
• Usually self-limiting, well tolerated, and needs no treatment. If symptomatic, atropine is an option; temporary pacing may be needed.
• Do not give amiodarone or other ventricular-suppressing drugs — they would further reduce the heart rate.

2.19 Defibrillation vs. synchronized cardioversion

2.20 Implantable cardioverter-defibrillator

• Indicated for patients who (1) survived SCD, (2) have spontaneous sustained VT, (3) have syncope with inducible VT or VF on EPS, or (4) are at high risk for future lethal dysrhythmias (e.g., cardiomyopathy).
• Lead placed via subclavian vein to the endocardium; pulse generator implanted subcutaneously, usually over the pectoral muscle on the nondominant side.

• Delivers a 25-joule or lower shock; recycles and repeats if unsuccessful. Also has antitachycardia and antibradycardia pacing — overdrive pacing can terminate SVT/VT and spare the patient painful shocks.
• A subcutaneous ICD (S-ICD) has no intracardiac electrodes and therefore no pacing capability; used for structural or congenital anomalies.
• Shock sensation is described as a blow to the chest. Expect fear of body image change, fear of recurrence, and anxiety about going home.

2.21 Pacemakers

• Circuit = battery-powered pulse generator with programmable circuitry + pacing lead(s) + myocardium. “Capture” means the muscle was stimulated to contract.
• Most are demand pacemakers: a sensing device inhibits firing when the HR is adequate, and a pacing device triggers when no QRS occurs within a preset time.
• Permanent: generator subcutaneous over the pectoral muscle on the nondominant side, leads placed transvenously. Indications include acquired AV block, second- and third-degree block, AF with slow ventricular response, bundle branch block, cardiomyopathy, HF, SA node dysfunction, symptomatic bradycardia of unknown cause, tachydysrhythmias.
• Cardiac resynchronization therapy (CRT) paces both ventricles (biventricular) to correct dyssynchrony in HF; may be combined with an ICD.
• Temporary types:transvenous (lead threaded to right atrium/ventricle, external generator; usually placed in ED or ICU), epicardial (leads attached during heart surgery and passed through the chest wall), and transcutaneous (noninvasive, bridges to transvenous or definitive therapy).
• TCP pad placement: one pad anterior at about the V4 position, the other on the back between the spine and left scapula at the level of the heart. Program the lowest current that achieves capture to minimize discomfort.
• Tell the patient TCP is uncomfortable — the muscle contractions as current crosses the chest wall are painful. Reassure that it is temporary, and provide analgesia and/or sedation if possible.

• Troubleshooting a temporary pacer: check that all connections are tight, confirm the generator has power, ensure pad-to-skin contact. Not capturing → turn up the milliamps and set 10 mA above capture; not sensing → turn up sensitivity. For either, placing the patient on the left side promotes lead contact with the epicardium.
• Insertion complications: infection, hematoma, pneumothorax, failure to sense or capture, septal perforation by the lead, end-of-life battery power. Preventive measures: prophylactic IV antibiotics, post-insertion chest x- ray to check lead placement and rule out pneumothorax, site observation, continuous ECG monitoring.
• After insertion the patient can be out of bed once stable; limit arm and shoulder activity on the operative side to avoid dislodging leads. Most patients are discharged the next day.

Covers: Lewis Ch. 39, p. 899-907

One switch separates the two shock therapies, and forgetting it is the classic exam trap. Everything else here is device safety and patient teaching.

Radiofrequency catheter ablation

Beyond the lecture guide — Radiofrequency ablation — not taught in the lecture.

• Uses electrical energy to burn away accessory pathways or ectopic foci in the atria, AV node, or ventricles, after EPS has located the source.
• Definitive treatment for tachydysrhythmias; the nonpharmacologic treatment of choice for atrial dysrhythmias with rapid ventricular rates and for AV nodal reentrant tachycardia refractory to drugs.
• Effective with a low complication rate. Post-procedure nursing care mirrors care after cardiac catheterization.

3.2 Rheumatic fever and rheumatic heart disease

• RF occurs 2-3 weeks after group A streptococcal pharyngitis. Rheumatic heart disease is the chronic scarring and deformity of valves that results.
• About 50% of RF episodes are rheumatic pancarditis, involving endocardium, myocardium, and pericardium.
• Valve leaflets swell and erode; vegetations form; leaflets thicken, commissures and chordae tendineae fuse, papillary muscle fibroses. Calcification → stenosis; incomplete closure → regurgitation. The mitral and aortic valves are most often affected.
• Aschoff's bodies — nodules formed by inflammatory reaction with collagen destruction; they fibrose into myocardial scar.
• Diagnosis by Jones criteria: 2 major, or 1 major + 2 minor, plus evidence of preceding group A strep infection.
• Major criteria:carditis (the most important — murmurs of mitral/aortic regurgitation or mitral stenosis, cardiomegaly and HF from myocarditis, pericarditis with muffled sounds/chest pain/friction rub), arthritis (monoarthritis, polyarthritis, or polyarthralgia — the most common finding, up to 75%, affecting knees, ankles, elbows, wrists), erythema marginatum (bright pink, nonpruritic, maplike macules on trunk and proximal extremities that intensify with heat; <10% of patients), subcutaneous nodules (small, hard, painless,

over extensor surfaces), Sydenham's chorea (involuntary movements of face and limbs, muscle weakness, speech and gait problems).

• Minor criteria: monoarthralgia, fever, elevated ESR and/or CRP, and a prolonged PR interval on ECG.
• Evidence of strep: elevated antistreptolysin-O titer, positive throat culture, or positive rapid antigen test.
• Treatment: antibiotics (IM benzathine penicillin G most widely used; cephalexin, clindamycin, or azithromycin if penicillin-allergic) plus salicylates, NSAIDs, and corticosteroids for fever and joint symptoms. Antibiotics do not change the course of acute disease or prevent carditis — they eradicate residual strep and prevent spread.
• Secondary prevention: RF without carditis needs prophylaxis until age 20 and a minimum of 5 years. Rheumatic carditis with residual heart disease needs lifelong prophylaxis.
• Teach patients to report excessive fatigue, dizziness, palpitations, unexplained weight gain, or exertional dyspnea. Position painful joints in alignment and apply heat for comfort.

Covers: Lewis Ch. 40, p. 909-919

Four inflammatory conditions, each affecting a different heart layer. Match the layer to the hallmark finding and most of these questions answer themselves.

Infective endocarditis

Beyond the lecture guide — Not taught in the lecture — the chapter's own material.

• About 50% of cases are Staphylococcus aureus. Others: Streptococcus viridans, coagulase-negative staphylococci, and HACEK organisms. Organisms form biofilms that shield them from immune defenses and antimicrobials.
• Subacute form affects preexisting valve disease over months; acute form strikes healthy valves and progresses rapidly.
• Three stages: bacteremia → adhesion → vegetation (fibrin, leukocytes, platelets, and microbes adhering to the valve).
• Main risk factors: prior IE, IV drug use, prosthetic valve, health care-associated infection from an intravascular device, and renal dialysis. Incidence is rising largely because of IV drug use.
• Embolization follows the side:left-sided vegetations travel to brain, kidneys, spleen, and extremities; right- sided lesions travel to the lungs → pulmonary emboli.

• Diagnostics: three blood cultures drawn over 1 hour from three different venipuncture sites; mild leukocytosis; elevated ESR and CRP; echocardiography shows vegetations. Duke Criteria guide diagnosis.
• Culture-negative IE suggests antibiotic use within the prior 2 weeks or an organism not detected by standard cultures.
• Treatment: 4-6 weeks of IV antibiotics based on culture results, with repeat cultures to confirm effectiveness. Persistent positive cultures mean wrong or inadequate antibiotics, an abscess, or a wrong diagnosis.
• HF occurs in up to 80% of aortic valve IE and 50% of mitral valve IE. Three reasons for valve surgery: valve dysfunction causing HF, prevention of embolization, or uncontrolled infection.
• Teaching: avoid people with infections and report cold/flu/cough symptoms; avoid fatigue and plan rest periods; good oral hygiene and regular dental visits; monitor temperature (persistent fever may mean the

antibiotic is ineffective); inform HCPs about the IE history before invasive procedures; refer for drug rehabilitation if IV drug use. Prevent immobility complications with compression stockings, ROM, and deep breathing/coughing every 2 hours.

• Antibiotic prophylaxis target groups: certain congenital heart disease, heart transplant recipients who develop valve disease, prior IE, prosthetic valve or prosthetic repair material. Procedures: dental manipulation of gums or tooth roots or puncturing oral mucosa; respiratory tract incisions, tonsillectomy, adenoidectomy; surgery involving infected skin or musculoskeletal tissue.

Acute pericarditis

Beyond the lecture guide — Pericarditis — not taught in the lecture.

• The pericardial space normally holds 10-15 mL of serous fluid. The pericardium anchors the heart, lubricates, and prevents excess dilation during diastole.
• Most often idiopathic or viral; about 20% follow cardiac injury. Post-MI (Dressler) pericarditis appears 4-6 weeks after transmural MI, more common after large anterior infarcts.
• Pain: progressive, severe, sharp; worse with deep inspiration and lying flat, relieved by sitting up and leaning forward. May radiate to neck, arms, or left shoulder — and characteristically to the trapezius (shoulder/upper back), which angina does not do.
• Hallmark: pericardial friction rub — scratching, grating, high-pitched; best heard at the lower left sternal border with the patient leaning forward. Often intermittent.
• To distinguish from a pleural rub, ask the patient to hold their breath — if the rub persists, it is cardiac.
• ECG: diffuse (widespread) ST elevation across many unrelated leads, present in about 90% of cases. In MI the ST changes are localized and evolve on serial ECGs; in pericarditis they do not evolve.
• Treatment: NSAIDs for pain and inflammation; corticosteroids for SLE-related, already-steroid-treated, or NSAID-unresponsive cases; antibiotics for bacterial cause; colchicine for pericarditis lasting more than 10 days or recurrent; aspirin after ST elevation MI. Keep the patient on bed rest with head of bed at 45 degrees and an overbed table for support. Give antiinflammatories with food or milk, avoid alcohol, consider a PPI.

Chronic constrictive pericarditis and myocarditis

Beyond the lecture guide — Constrictive pericarditis and myocarditis — not taught.

• Chronic constrictive pericarditis: fibrosis, thickening, and calcification encase the heart and restrict ventricular filling. Causes include tuberculosis, recent heart surgery, mediastinal radiation, or idiopathic. Manifestations mimic HF and cor pulmonale — dyspnea on exertion, peripheral edema, ascites, fatigue, anorexia, weight loss; the most prominent finding is JVD. Treatment of choice is pericardiectomy; diuretics for nonsurgical candidates.
• Myocarditis: focal or diffuse inflammation of the myocardium. Coxsackie A and B viruses are the most common causes. The agent invades myocytes → cellular damage and necrosis → immune response → autoimmune response → further myocyte destruction.
• Early (viral) signs: fever, fatigue, malaise, myalgias, pharyngitis, dyspnea, lymphadenopathy, nausea and vomiting. Cardiac signs appear 7-10 days after the viral infection. Pericarditis often accompanies it (pleuritic pain, friction rub, effusion). Late signs are those of HF: S3, crackles, JVD, syncope, peripheral edema, angina.
• Endomyocardial biopsy gives histologic confirmation and is most diagnostic in the first 6 weeks of acute illness. The virus is present in tissue and pericardial fluid only during the first 8-10 days.
• Treatment: symptom management — ACE inhibitors and β-blockers, diuretics, nitroprusside/milrinone for afterload reduction if not hypotensive, anticoagulation for low EF. Digoxin is used with caution because myocarditis predisposes to drug-related dysrhythmias and toxicity. Immunosuppressives for autoimmune cause.
• Nursing: decrease cardiac workload — semi-Fowler's position, space activity and rest, quiet environment. Monitor for infection if immunosuppressed. Some patients progress to dilated cardiomyopathy and may need transplant.

3.3 Mitral valve disorders

3.6 Aortic valve disorders

3.8 Tricuspid and pulmonic disorders

• Tricuspid regurgitation — primary (IE or congenital) is less common; secondary comes from RV dilation due to pulmonary hypertension, cor pulmonale, or outflow obstruction. JVD, enlarged liver, and peripheral edema appear only when severe. Poor prognosis in severe TR.
• Tricuspid stenosis — usually from rheumatic fever. Fluttering discomfort in the neck, fatigue, possible right upper quadrant pain; diastolic low-pitched murmur that increases in intensity during inspiration.
• Pulmonic regurgitation — often asymptomatic; crescendo-decrescendo murmur; causes include pulmonary hypertension, surgical repair of tetralogy of Fallot, congenital valve disease.
• Pulmonic stenosis — usually congenital; causes RV hypertension and hypertrophy; largely asymptomatic until adulthood, then symptoms resemble AS (syncope, dyspnea, angina).

3.10 Diagnosis and management

• Echocardiogram shows valve structure, function, and chamber size — TEE and Doppler color-flow help diagnose and monitor progression. Chest x-ray shows heart size, altered pulmonary circulation, and calcification. ECG shows rate, rhythm, ischemia, or hypertrophy. Heart catheterization measures chamber pressures, gradients across valves, and orifice size.
• Conservative therapy targets prevention of HF exacerbations, pulmonary edema, thromboembolism, and recurrent RF and IE: prophylactic antibiotics, sodium restriction, vasodilators (cautiously in AS), positive inotropes, diuretics, β-blockers, anticoagulation, antidysrhythmics.

• Percutaneous transluminal balloon valvuloplasty (PTBV) splits fused commissures with a balloon-tipped catheter threaded from the femoral vessel. The Inoue single-balloon technique is most popular. It is not a permanent fix for stenosis.
• Valve repair is preferred over replacement when appropriate — lower operative mortality, often used for mitral or tricuspid disease, but it may not restore total valve function. Options: open surgical valvuloplasty, minimally invasive approaches, and annuloplasty (reconstruction of the annulus, with or without a prosthetic ring).
• TAVR (transcatheter aortic valve replacement) is an option for severe symptomatic AS; over 90% are done transfemorally. Transcatheter edge-to-edge repair is available for severe MR in very-high-risk surgical patients.

• Nursing care: HF is the most common reason for ongoing medical care. Design activities around limitations — conserve energy, set priorities, plan rest periods, limit activities causing fatigue and dyspnea, and avoid strenuous exercise because damaged valves cannot handle the increased cardiac output. Discourage tobacco. Consider vocational counseling for physically demanding jobs.
• Teach patients on warfarin after valve replacement to have INR checked regularly; report signs of infection, HF, or bleeding, and any planned invasive or dental work; wear a Medic Alert device and carry the manufacturer's valve information card.

Covers: Lewis Ch. 40, p. 919-925

Two failures are possible at any valve: it won't open (stenosis) or it won't close (regurgitation). Stenosis backs pressure up behind the valve; regurgitation sends volume backward.

• Stenosis — the opening is narrowed by limited leaflet motion; forward flow is impaired and a pressure difference develops across the valve. The greater the difference, the greater the stenosis.
• Regurgitation (incompetence, insufficiency) — incomplete closure allows backward flow.
• Congenital conditions are the most common cause in children and teens. In adults: endocarditis, rheumatic heart disease, hypertension, and autoimmune disorders. Aortic stenosis and mitral regurgitation are common in older adults.