The Heart Factory

💥 The Supply Lines: Coronary Arteries

Every factory needs its own fuel supply lines, and the heart is no exception. The coronary arteries are the heart’s personal blood supply, delivering oxygen and nutrients directly to the cardiomyocyte factory workers in the myocardium. Even though the heart pumps blood to the entire body, it cannot use the blood that flows through its chambers. Instead, it depends entirely on the coronary arteries that branch off the aorta and wrap around the outside of the heart. If any of these supply lines become blocked, usually by a buildup of fatty plaque called atherosclerosis, the cardiomyocytes downstream are starved of oxygen. Within about 20 minutes of complete blockage, those cells begin to die. This is a myocardial infarction, commonly known as a heart attack.

The two main coronary arteries are the right coronary artery and the left main coronary artery. The right coronary artery supplies the right side of the heart, the inferior portion of the left ventricle, and critically, the SA and AV nodes, which control heart rhythm. This means that a blockage of the right coronary artery often causes dysrhythmias like bradycardia or heart blocks. The left main coronary artery quickly splits into two major branches. The left anterior descending artery, often called the LAD or the “Widow Maker,” is the most dangerous vessel because it supplies the entire anterior wall of the left ventricle, the ventricular septum, and the apex. A blockage here can destroy a massive portion of the heart’s main pumping chamber. The circumflex artery wraps around the left side supplying the left atrium and the lateral and posterior walls of the left ventricle. Here is a quick reference for each artery:

• Right Main Coronary Artery: Supplies the right atrium and ventricle, the inferior portion of the left ventricle, the posterior septal wall, and the SA and AV nodes.
• Left Main Coronary Artery: Splits into two major branches:
  • Left Anterior Descending (LAD) Artery: Supplies the anterior wall of the left ventricle, the anterior ventricular septum, and the apex. Sometimes called the "Widow Maker" because blockage here is very dangerous!
  • Circumflex Artery: Supplies the left atrium and the lateral and posterior surfaces of the left ventricle.

⚠️ CRITICAL: Electrolyte Imbalances & the Heart

Electrolyte imbalances can cause life-threatening cardiac electrical instability! At the CELL FACTORY level, electrolytes are the ions that flow through the security gates (ion channels). If levels are off, the gates malfunction!

📈 Seeing Electrolyte Changes on ECG: A Visual Recognition Guide

At the cell factory level, electrolytes are the raw materials that flow through the security gates (ion channels). When these materials are out of balance, the gates malfunction and the ECG shows characteristic patterns that you can learn to recognize. This is a heavily tested NCLEX skill.

Hyperkalemia (too much potassium outside the cell) produces tall, tent-shaped, peaked T waves. Think of it as the potassium gates being overwhelmed: the repolarization phase becomes exaggerated. As hyperkalemia worsens, the QRS widens and the P waves flatten and eventually disappear. Severe hyperkalemia can cause asystole and death.

Hypokalemia (too little potassium) produces flattened T waves, prominent U waves (a small wave after the T wave that is normally invisible), and ST depression. The cell cannot properly repolarize because there is not enough potassium to exit. Critically, hypokalemia increases the risk of digoxin toxicity because digoxin and potassium compete for the same binding site on the Na⁺/K⁺-ATPase pump.

Hypocalcemia produces a prolonged QT interval because the plateau phase (Phase 2) of the action potential is extended when there is insufficient calcium. A prolonged QT interval puts the client at risk for a dangerous dysrhythmia called Torsades de Pointes, which can degenerate into V-Fib.

⚠️ What Are Dysrhythmias?

Dysrhythmias occur when the electrical conduction system malfunctions. At the cell factory level, this means the cardiomyocyte communication network has broken down. Cells may fire too fast because abnormal pacemaker sites are generating impulses, or too slow because the normal pacemaker sites are damaged or blocked. The heart may beat irregularly because multiple sites are competing to send signals, or the rhythm may originate from the wrong location entirely, such as from the ventricles instead of the SA node. Common causes include hypoxia, which starves the cells of oxygen and disrupts their electrical behavior, electrolyte imbalances especially potassium and magnesium, adverse effects of medications including digoxin and antidysrhythmics, and damage from cardiac procedures or myocardial infarction.

The primary nursing concern with any dysrhythmia is whether the rhythm affects how well the heart can pump blood, which is called cardiac output. A rhythm that looks alarming on a monitor might be tolerated well by one client, while a less dramatic-looking rhythm might cause dangerous hemodynamic instability in another. This is why NCLEX emphasizes clinical judgment: always observe the client first, not just the monitor. The overall goal of treatment is to restore a normal rate and rhythm that maintains adequate cardiac output and tissue perfusion. For the NCLEX Next Generation clinical judgment model, dysrhythmias are a perfect example of recognizing cues, analyzing cues, and taking action.

💀 LIFE-THREATENING DYSRHYTHMIAS: Immediate Recognition Required!

📈 Learning to SEE Dysrhythmias: Your Visual Recognition Guide

As an LPN, you will not be expected to independently interpret ECGs, but you MUST be able to visually recognize life-threatening rhythms and call for help immediately. This is a Recognize Cues skill. The difference between recognizing ventricular fibrillation in seconds versus hesitating for even one minute can be the difference between life and death. VF is fatal within 3 to 5 minutes without treatment.

Each rhythm has a signature visual pattern. Normal sinus rhythm looks organized and predictable: a small rounded P wave, followed by a tall sharp QRS complex, followed by a rounded T wave, repeating in an even pattern like a steady heartbeat. As rhythms become more dangerous, they become more chaotic, faster, wider, or flatter.

Atrial fibrillation loses its P waves entirely because the atria are quivering instead of contracting. The baseline looks wavy and the rhythm is irregularly irregular, meaning there is no pattern to the irregularity. Ventricular tachycardia shows very wide QRS complexes that fire rapidly because the impulse originates in the ventricle rather than the normal conduction pathway. Ventricular fibrillation shows pure chaos with no identifiable waves at all, just a wildly undulating line. Asystole is the most sobering: a flat line with no electrical activity whatsoever.

Study the visual gallery below carefully. Train your eyes to immediately spot these patterns. On NCLEX, you may see a rhythm strip image and be asked to identify the appropriate nursing action.

⚠️ Pulseless Electrical Activity (PEA)

Pulseless electrical activity, or PEA, is one of the most dangerous and deceptive situations in cardiac care, and it is a heavily tested NCLEX concept. In PEA, the cardiac monitor shows organized electrical activity that may look completely normal, with identifiable P waves, QRS complexes, and T waves, but there is NO actual mechanical contraction of the heart. The cardiomyocyte factories are receiving the electrical signal, but they are not responding with contraction. At the cell factory level, this disconnect can occur when the cells are too damaged, too oxygen-starved, or too depleted of calcium and ATP to physically contract even though the electrical wiring is intact. Think of it like a factory alarm going off but all the workers are incapacitated and cannot respond.

The critical clinical lesson for the NCLEX is this: never trust the monitor alone. PEA is the most common dysrhythmia seen immediately after defibrillation, so after every shock delivery, you must check for a pulse. If the monitor shows a rhythm but there is no pulse, the client is in PEA and requires immediate CPR and epinephrine. PEA is a non-shockable rhythm, which means defibrillation will NOT help. You cannot shock cells into contracting when the problem is mechanical failure, not electrical chaos. The treatment is high-quality CPR, IV epinephrine every 3 to 5 minutes, and identifying and treating the underlying cause, which often includes hypovolemia, hypoxia, hydrogen ion excess or acidosis, hypokalemia or hyperkalemia, hypothermia, cardiac tamponade, tension pneumothorax, toxins, or thrombosis. Always remember: check the patient, not just the monitor!

🚨 Clinical Judgment in Action: The Cardiac Emergency Decision Pathway

When you walk into a room and find a client who appears unresponsive, your brain must follow a rapid, systematic decision pathway. The Next Generation NCLEX tests this through the Clinical Judgment Model: you Recognize Cues (what do you see?), Analyze Cues (what do they mean?), Prioritize Hypotheses (what is most likely and most dangerous?), and Generate Solutions (what do you do FIRST?).

The very first step is always to check responsiveness: tap the client and ask loudly, “Are you okay?” If there is no response, call for help immediately and activate the emergency response system. Next, check the carotid pulse for a maximum of 10 seconds. Do not waste precious time with prolonged pulse checks. If there is no pulse, you have entered a cardiac arrest situation and must determine whether the rhythm is shockable or non-shockable.

The two shockable rhythms are ventricular fibrillation and pulseless ventricular tachycardia. Both show electrical activity that can be “reset” with defibrillation. The two non-shockable rhythms are asystole (no electrical activity at all) and pulseless electrical activity (the monitor shows a rhythm but there is no mechanical contraction producing a pulse). For non-shockable rhythms, you provide CPR and epinephrine. Shocking a flatline accomplishes nothing because there is no electrical activity to reset.

If the client has a pulse but is hemodynamically unstable (hypotension, altered level of consciousness, chest pain), and the rhythm is ventricular tachycardia, the treatment is synchronized cardioversion plus antidysrhythmic medications. Always re-evaluate after every 2 minutes (5 cycles of CPR) or after any intervention.

⚠️ DIGOXIN (Lanoxin) — High-Alert Medication!

Digoxin, also known by the brand name Lanoxin, is one of the most heavily tested medications on the entire NCLEX examination. It is classified as a cardiac glycoside and is considered a high-alert medication because even small errors in dosing can be fatal. At the cell factory level, digoxin works by blocking the sodium-potassium-ATPase pump on the cardiomyocyte membrane. When this pump is blocked, sodium accumulates inside the cell, which causes the sodium-calcium exchanger to bring in more calcium. More calcium reaches the sarcomeres, the contractile machinery, and the cell contracts more forcefully. This is why digoxin is called a positive inotrope, meaning it increases the force of contraction. It also slows conduction through the AV node, which reduces heart rate and makes it useful for controlling the ventricular rate in atrial fibrillation.

The single most critical nursing action with digoxin is to check the apical pulse for one full minute before every dose. If the heart rate is below 60 beats per minute in an adult, you must HOLD the medication and notify the PHCP immediately. The therapeutic serum level for digoxin is 0.5 to 2.0 nanograms per milliliter, with lower levels now preferred to minimize toxicity risk. Always check the potassium level too, because hypokalemia, or low potassium, dramatically increases the risk of digoxin toxicity since digoxin and potassium compete for the same binding site on the pump.

Action at the Cell Factory Level: Digoxin activates contractile proteins (sarcomeres), increasing contraction force (positive inotrope). It also slows conduction through the AV node, reducing heart rate. Used for heart failure and atrial dysrhythmias (A-Fib, SVT).

🚨 DIGOXIN TOXICITY SIGNS (NCLEX FAVORITE!):

• Early signs (GI): Anorexia, nausea, vomiting, diarrhea
• Then: Heart rate abnormalities (bradycardia, heart block, PVCs)
• Visual disturbances: Diplopia, blurred vision, YELLOW-GREEN HALOS, photophobia
• CNS: Drowsiness, confusion, fatigue, weakness

🚨 CRITICAL NURSING ACTIONS:

• Check APICAL pulse for 1 FULL MINUTE before giving. Hold if less than 60 bpm and notify PHCP!
• Therapeutic range: 0.5 to 2.0 ng/mL (low end preferred to avoid toxicity)
• Monitor POTASSIUM level! Hypokalemia INCREASES digoxin toxicity risk!
• Antidote: Digoxin Immune Fab for severe toxicity
• Contraindicated in ventricular dysrhythmias and 2nd or 3rd degree heart block
• Older adults are MORE sensitive to digoxin toxicity!

🚨 Recognizing Digoxin Toxicity: The Warning Signs Appear in a Specific Order

One of the most heavily tested NCLEX topics is recognizing digoxin toxicity. The key to this question type is understanding that the symptoms appear in a predictable order, which helps you identify toxicity before it becomes life-threatening. The GI symptoms always appear FIRST, because the GI tract is extremely sensitive to digoxin. The client will complain of loss of appetite (anorexia), nausea, vomiting, and diarrhea. Many students miss this cue because they attribute nausea to other causes, but on NCLEX, any client taking digoxin who develops GI symptoms should be suspected of toxicity until proven otherwise.

The cardiac symptoms appear next: bradycardia (heart rate dropping below 60 bpm), new onset of heart block, and new or worsening PVCs. This is why the #1 nursing action before giving digoxin is to check the apical pulse for one full minute. If the heart rate is below 60 bpm, HOLD the dose and notify the PHCP.

The visual disturbances are the classic textbook finding: yellow-green halos around lights, blurred vision, diplopia (double vision), and photophobia. While these are the most memorable symptoms, they actually appear after the GI and cardiac signs. Finally, CNS symptoms like drowsiness, confusion, and fatigue represent severe toxicity.

The therapeutic range for digoxin is 0.5 to 2.0 ng/mL, with the lower end now preferred to minimize toxicity risk. The antidote for severe toxicity is Digoxin Immune Fab (Digibind). Older adults are at particularly high risk because of decreased renal function, and the maximum dose is often reduced to 0.125 mg daily in elderly clients.

⚠️ Amiodarone (Cordarone) — Class III Special Considerations

Amiodarone is the most powerful and most dangerous antidysrhythmic drug available, and it is frequently tested on the NCLEX. It is classified as a Class III potassium channel blocker, but it is unique because it actually has properties of all four Vaughan-Williams classes. At the cell factory level, its primary action is to block potassium channels during Phase 3 of the action potential. By slowing potassium exit from the cell, amiodarone prolongs the refractory period, which is the time the cardiomyocyte must wait before it can fire again. This prevents the rapid, chaotic firing that occurs in life-threatening dysrhythmias like ventricular tachycardia and ventricular fibrillation.

Amiodarone is so powerful that it is often initiated only in a critical care setting. It has a remarkably long half-life of 40 to 55 days, meaning the drug stays in the body for weeks to months after it is discontinued. This extended presence means side effects may not appear for days or weeks after starting the drug, and they persist long after the drug is stopped. The most serious adverse effect is pulmonary toxicity, which can cause irreversible lung damage. Amiodarone also deposits in the skin and eyes over time, causing photosensitivity, a bluish discoloration of the face and neck, and corneal microdeposits that require regular eye examinations. Here are the specific nursing considerations:

• Very powerful! Often given only in critical care units initially.
• Side effects: photosensitivity, nausea, vomiting, dizziness, fatigue, hypotension.
• Monitor respiratory status! Can cause pulmonary complications.
• Teach patients to wear dark glasses and protective clothing (light sensitivity).
• Long-term use may cause bluish discoloration of face, neck, or arms (reversible).
• Schedule eye examinations every 6 to 12 months (corneal microdeposits).
• Side effects may not appear until days or weeks after starting the drug.

⚡ Cardioversion: Synchronized Countershock

Cardioversion uses synchronized countershock to convert an undesirable rhythm to a stable rhythm. At the cell factory level, here is what is happening: the electrical signal is being delivered in a carefully timed burst that coincides with the R wave of the ECG. The defibrillator literally watches the ECG and waits for the R wave before firing. Why does this timing matter so much? Because the T wave represents the vulnerable period when the ventricular cardiomyocytes are in the middle of repolarization. Their potassium channels are open and their electrical state is unstable. If a shock hits during the T wave, it could trigger every cardiomyocyte to fire chaotically, converting an organized rhythm into deadly ventricular fibrillation. Synchronization prevents this by ensuring the shock arrives when the cells are in a stable electrical state.

Cardioversion can be performed as an elective procedure for stable tachydysrhythmias that are resistant to medication, or as an emergency procedure for hemodynamically unstable rhythms. When it is performed electively for atrial fibrillation or atrial flutter, the client must receive anticoagulant therapy for four to six weeks beforehand, and a transesophageal echocardiogram is performed to rule out clots in the atria. The energy used in cardioversion is lower than in defibrillation. Safety is paramount during the procedure: oxygen must be stopped to prevent fire, the client's skin must be clean and dry, and the nurse must verify three times that absolutely no one is touching the bed or the client before the shock is delivered. Post-procedure, the priority nursing action is airway and breathing monitoring.

Key Points:

• Uses LOWER energy than defibrillation.
• Can be elective (for stable tachydysrhythmias) or emergent (for unstable VT or SVT).
• Elective A-Fib/Flutter: Client receives anticoagulant therapy for 4-6 weeks BEFORE and TEE to rule out clots.
• If elective, hold digoxin 48 hours before to prevent postcardioversion ventricular irritability.
• STOP oxygen during procedure (fire hazard!).
• Ensure NO ONE is touching the bed or client! (Check 3 times!)
• Post-procedure PRIORITY: Airway and breathing data collection!

⚡ Defibrillation: Asynchronous Countershock

Defibrillation is an asynchronous countershock used exclusively for two pulseless rhythms: ventricular fibrillation and pulseless ventricular tachycardia. These are the only two shockable rhythms, and remembering this is a critical NCLEX skill. Unlike cardioversion, defibrillation is NOT synchronized to the R wave, and here is why: in ventricular fibrillation, the cardiomyocytes are firing in complete chaos with no organized rhythm at all. There is no identifiable R wave to synchronize to. The goal of the shock is to simultaneously depolarize every single cardiomyocyte in the heart at once, essentially resetting the entire electrical system to zero. The hope is that the SA node will then resume its role as the master pacemaker and restart an organized rhythm. Think of it like rebooting a factory’s entire computer system when every machine is running haywire. You shut everything down at once and let the master controller boot up fresh.

The energy used is higher than cardioversion, typically 120 to 200 joules with a biphasic defibrillator or 360 joules with a monophasic unit. After delivering one shock, CPR must be immediately resumed for 2 minutes, which is 5 cycles of 30 compressions and 2 breaths, before rechecking the rhythm. The same safety rules apply: stop oxygen to prevent fire, ensure no one is touching the bed or client, and clear three times before delivering the shock.

• Energy: 120-200 joules (biphasic) or 360 joules (monophasic).
• After one shock, immediately resume CPR for 2 minutes (5 cycles). Then recheck rhythm.
• Stop oxygen! Ensure no one is touching bed or client!
• Pad placement: One at 3rd intercostal space right of sternum. Other at 5th intercostal space left midaxillary line. Avoid breast tissue!

📌 Where Do the Pads Go? Visualizing Defibrillator Placement

When a client is in ventricular fibrillation or pulseless ventricular tachycardia, every second counts. The defibrillator pads must be placed in the correct position so the electrical current travels directly through the heart muscle. Think of it this way: you are creating a pathway for electricity to flow between the two pads, and the heart needs to sit right in the middle of that path.

The anterior pad (Pad 1) is placed at the 3rd intercostal space to the RIGHT of the sternum. The lateral pad (Pad 2) is placed at the 5th intercostal space at the LEFT midaxillary line. This diagonal placement ensures the electrical current crosses through the bulk of the ventricular muscle mass.

Critical safety reminders: Apply firm pressure of at least 25 pounds to ensure good skin contact. Avoid placing pads over breast tissue because fat does not conduct electricity well. Remove any nitroglycerin patches (they can cause burns). Make sure the chest is dry. And most importantly: STOP oxygen delivery during the shock because oxygen supports combustion and creates a fire hazard! Ensure nobody is touching the bed or the client before firing. Announce “Clear!” and visually verify three times: “I am clear, you are clear, everybody is clear.”

⚡ Seeing the Difference: Synchronized vs Asynchronous Shock

Students often confuse cardioversion and defibrillation because both deliver an electrical shock to the heart. The difference comes down to timing and purpose. In cardioversion, the defibrillator machine watches the ECG and waits for the R wave before delivering the shock. This “synchronization” ensures the shock avoids the T wave, which is the vulnerable period when shocking could trigger ventricular fibrillation. The client usually still has an organized rhythm and a pulse, and the goal is to reset that rhythm to normal sinus.

In defibrillation, there is NO synchronization because the heart has no organized rhythm to synchronize to. Ventricular fibrillation is pure chaos, so the machine fires immediately without waiting. The goal is to stun all the chaotic electrical activity at once, giving the SA node a chance to restart as the primary pacemaker.

At the cell factory level, think of it this way: cardioversion is like a factory manager clapping loudly to get a disorganized but still functioning team back on schedule. The manager waits for the right moment to clap so workers do not drop fragile items (avoiding the T wave). Defibrillation is like pulling the fire alarm in a factory that has descended into complete pandemonium. There is no “right moment” because everything is already in chaos, so you just hit the alarm immediately and hope everyone resets.