Welcome to the show! I'm Caitlin Hope with Derek Mendoza, Karen Whitaker, and Professor Heather Murphy, and I want to start with a patient who looked... honestly, pretty fine. Sitting up, talking, skin not terrible, telling me, "It's just a little pressure." [short pause] Twelve-lead EKG comes back with ischemic changes, and suddenly the whole room changes. [warmly] That is SUCH a nursing moment. The patient can be chatting with you while the myocardium is already saying, very quietly, "I am not getting enough oxygen." [reflective] Yeah. I always think cardiac nursing gets taught as separate boxes: hypertension over here, coronary artery disease (CAD) over there, dysrhythmias somewhere else. But bedside? It's really one big question: is oxygen getting where it needs to go? To the heart muscle, to the brain, to the kidneys, to the whole body. Exactly. Perfusion is the thread that ties the whole thing together. Hypertension increases the workload. Coronary artery disease narrows the pipes. Angina is the warning signal from ischemia. Acute coronary syndrome is when that mismatch becomes dangerous fast. And dysrhythmias can tank cardiac output even if the blood vessels are fine. Different mechanism, same consequence: tissues do not get what they need. [quick, crisp] And that is why nurses cannot wait for dramatic collapse before they get serious. Cardiac patients often declare themselves LATE. Chronic hypertension can be a total silent creep. Silent ischemia can happen with no pain at all, especially in patients with diabetes because of neuropathy. So if you're waiting for somebody to clutch their chest movie-style, you're late. Wait -- that phrase "silent ischemia" is one I want listeners to hang onto. No chest pain, but still ischemia, same prognosis as ischemia with pain. That's the part that always makes me sit up straighter. Yes, and NCLEX loves that concept. If a patient reports unusual fatigue, dyspnea, or just "I don't feel right," don't dismiss it because they are not reporting pain. The heart does not care whether the patient used the word pain. Ischemia is ischemia. [enthusiastic] I tell students to think of the cardiovascular system like delivery logistics. The body ordered oxygen. The heart has to pump it, the vessels have to carry it, and the rhythm has to keep the whole route on schedule. Hypertension stresses the delivery trucks. CAD narrows the roads. A dysrhythmia scrambles the dispatch center. [laughs] I love that. And I use a tiny mental sticky note on shift: looks okay does NOT mean is okay. If their blood pressure has been high for years, if they've got risk factors, if their symptoms are changing, if they are sweaty or short of breath or restless, I care. And that restlessness piece matters. In the ER I'd sometimes see this before anything else. Not a dramatic symptom list -- just a patient who couldn't get comfortable, had this unsettled look, maybe a little diaphoresis, maybe saying the pain was "indigestion." Those soft cues can be the first breadcrumb. [matter-of-fact] So the nursing lens for this whole episode is early recognition. Recognize cues, analyze them, prioritize quickly. Because when perfusion starts to fail, especially in acute coronary syndrome or unstable rhythms, minutes matter. Time is muscle in MI, and time is brain when cardiac output drops. And I want students to hear this with confidence, not fear. You do not need to know everything in the first ten seconds. You need to notice the right clues in the first ten seconds: what is the blood pressure, what is the pulse, what does the patient look like, what is the oxygen saturation, what does the rhythm look like, what changed? Right. That's the whole game. Not perfection -- pattern recognition. If the pattern says oxygen delivery is threatened, you move. Let's build the setup, because hypertension and CAD don't just appear out of nowhere. Hypertension is a massive cardiovascular risk factor, affects about 45 percent of adults in the United States, and as blood pressure rises, so does risk for MI, heart failure, stroke, renal disease, and retinopathy. Forty-five percent. That's almost every other adult. That's not some rare board question disease -- that's your waiting room. And with hypertension, I want students to picture afterload. The ventricle is pushing blood against greater pressure in the arterial system. Over time that chronic pressure damages the endothelium. Once the endothelial lining is injured, it becomes much easier for atherosclerosis to begin: lipids accumulate, fatty streak forms, collagen covers it into a fibrous plaque, the lumen narrows, blood flow drops, and if that plaque ruptures, a thrombus can form. That is the bridge from hypertension to coronary artery disease. [quickly] So if you want the short version: high pressure beats up the vessel wall, and damaged vessel walls are a great place for plaque to set up camp. Exactly. And CAD is plaque buildup in the coronary arteries. Once the coronary vessel is narrowed enough, the heart can meet oxygen demand at rest maybe... but not during exertion, stress, pain, fever, all those moments when demand goes up. Over time this can lead to a diagnosis of stable angina. The patient will have chest pain that occurs when the heart requires more oxygen than it usually does, such as during exercise. On an EGK strip, they may slight changes but at rest the EKG returns to normal, which is why this is called "stable" angina. The patient will have intermittent symptoms but will usually feel better at rest. Nitroglycerin also sometimes does the trick. The cool thing about our body is that it compensates for clogged or occluded vessels using collateral circulation. In other words, the vessels create detours around the occluded vessels to allow blood flow to go around the blockage. These are much smaller vessels though so they cannot handle a lot of pressure. In other words, they are helpers but not healers. Now risk factors -- because bedside teaching gets sloppy here. We say "lifestyle changes" and leave it fuzzy. Let's not do that. Modifiable risks for CAD and hypertension include tobacco use, diabetes, high serum lipids, obesity, physical inactivity, stress, substance use, excess dietary sodium for hypertension, and, big one, poor control of the stuff you already know about. And social determinants of health belong in that conversation too. Lack of access to care, poverty, chronic stress, safe housing, education, resources for food and medications -- these shape whether a patient can control blood pressure or cholesterol. It is not just "try harder." [softly] I'm glad you said that. I grew up seeing family members delay care because of cost and work schedules. So when we ask, "Are you taking your meds?" sometimes the real question is, "Can you afford them, and do you have a way to refill them, and do you work nights and sleep four broken hours?" And assessment should reflect that reality. A complete history includes lifestyle habits, occupation, stress exposure, shift work, other health conditions, family history of CAD or MI, medications, and social environment. That is not fluff. That is cardiac risk assessment. Let's do diagnostics, because this is very NCLEX and very bedside. Blood pressure technique matters. No smoking, exercise, or caffeine for 30 minutes before. Let the patient rest quietly for 5 minutes. No talking. Use the right cuff size. Arm at heart level. Take it in both arms on initial assessment, and if one arm is higher, use the higher arm for future checks. Also orthostatic vital signs. Supine for 5 minutes, then standing, measure at 1 minute and 3 minutes. Abnormal is a systolic drop of 20 mm Hg or more, diastolic drop of 10 mm Hg or more, or heart rate increase of 20 beats per minute or more, especially with dizziness or lightheadedness. For HTN workup and organ damage, think renal function, urinalysis, BMP, CBC, serum lipid profile, uric acid, ECG, and eye exam. If needed, echo, liver function tests, TSH. And for CAD specifically: lipid panel -- total cholesterol, LDL, HDL -- ECG, cardiac cath as the gold standard for coronary anatomy, stress testing, and cardiac biomarkers when ACS is in the picture. I like that combo in my head: pressure check, vessel damage check, organ damage check. BP, lipids, ECG, kidneys, eyes. It gives me a framework. That's a good framework. Because hypertension is called the silent killer for a reason. Patients are often asymptomatic until target-organ damage is already happening. And then years later they show up with CAD, LV hypertrophy, stroke history, kidney disease... and everybody acts surprised. The body usually gave us the numbers first. Remember that untreated, hypertensive crisis can occur which can lead to organ disease and worst case scenario, MI or aortic dissection. If you hypertensive patient has sudden extreme back pain, be concerned about major aorta damage and get help fast. Okay, here's the distinction students mix up ALL the time, so I'm gonna do this in clean little boxes. Stable angina: predictable chest pain or pressure when myocardial oxygen demand goes up, like exercise, stress, or emotional upset. It lasts a few minutes, follows a similar pattern over time, and gets better with rest, calming down, or sublingual nitroglycerin. So predictable is the keyword. Same staircase, same chest pressure, same relief after a couple minutes of rest. That's stable angina. Yes. Also, stable angina is ischemia, not infarction. On ECG you may see ST-segment depression or T-wave inversion during the episode, but when blood flow is restored and pain resolves, the ECG can return to baseline. As Professor Murphy mentioned earlier, the patient may not even call it pain. It may feel more like pressure, heaviness, or discomfort. Now let's talk about UNSTABLE angina. This is angina, even at rest. Or angina that's happening more often, lasting longer, or happening with less effort than before. Pain lasting more than 10 minutes. Unpredictable. Immediate treatment needed. That "less effort than before" clue is sneaky. The patient says, "I used to get this walking three blocks, now it happens walking to the bathroom." That's the story change. Exactly. And unstable angina is part of acute coronary syndrome. Biomarkers are negative in unstable angina, which is a huge distinction. Ischemia is present, but necrosis has not happened enough to release troponin. Now NSTEMI. NSTEMI means non ST elevation myocardial infarction. Similar symptoms to unstable angina -- chest pain at rest or worsening pattern -- but cardiac markers are elevated. Troponin rises because now you have myocardial injury, myocardial necrosis, without ST elevation on the ECG. [emphatic] This is the clean test tip: NSTEMI equals NO ST elevation, BUT troponins ARE up. Partial occlusion is the usual picture. Let me try saying it back. Unstable angina and NSTEMI can both look like rest pain or changing angina. The separator is troponin: negative for unstable angina, positive for NSTEMI. Is that fair? That is exactly fair. And STEMI is the one with ST-segment elevation in two adjoining leads, usually from total coronary occlusion. That is abrupt disruption of blood flow to an area of the heart. Emergency reperfusion is the goal. And STEMI is not just "more chest pain." It means artery closed, myocardium dying. Heart muscle becomes hypoxic within about 10 seconds of oxygen and glucose deprivation. Cells are viable around 20 minutes, but damage becomes irreversible if blood flow is not restored and collateral circulation is not enough. Ten seconds and 20 minutes -- those are the numbers that change the room. That's why "time is muscle" isn't a just cute slogan. It's literal. Yep. And here's the rapid sort in real life. ST elevation in two contiguous leads? Think STEMI until proven otherwise. No ST elevation, but symptoms fit acute coronary syndrome (ACS)? Check biomarkers. Troponin increases about 4 to 6 hours after onset of MI, peaks around 10 to 24 hours, and returns to baseline over 10 to 14 days. Cardiac-specific troponins are better indicators of MI than CK-MB or myoglobin. NCLEX likes that too. Troponin is the star. Clinical manifestations of MI are also worth hearing out loud. Severe chest pain not relieved by rest, position change, or nitrates. Heaviness, pressure, tightness, burning, constriction, crushing. Often substernal or epigastric, can radiate to neck, jaw, arms, or back. Often more than 20 minutes. Women and older adults may present atypically. Diabetic patients may have no pain at all. Add sympathetic signs: diaphoresis, elevated heart rate and blood pressure early, cool clammy skin, ashen look. Then later if cardiac output drops, blood pressure can fall. You might hear crackles with left ventricular dysfunction, or see JVD and edema with right-sided involvement. This is where I tell students to stop chasing the perfect chest pain script. If your patient has pressure, diaphoresis, nausea, dyspnea, maybe they're pale and saying they feel awful -- treat that story seriously, even if they don't say "elephant on my chest." Acute care priorities: position upright, give oxygen as indicated, assess vital signs, heart sounds, lung sounds, provide pain relief with nitroglycerin and IV opioid such as morphine if needed, obtain cardiac biomarkers, reduce anxiety, get the 12-lead ECG, start IV access, and place on cardiac monitor. And medications in ACS? Aspirin early unless contraindicated. Nitroglycerin. Beta blockers when appropriate. For unstable angina and NSTEMI, heparin is part of management. Statins are in the mix too. For reperfusion, percutaneous coronary intervention or PCI is first-line when available. This is done in a specialized cardiac cath lab. In a PCI, a catheter is inserted usually into the groin and is fed into the coronary arteries to the blocked area. A balloon may be inflated to open up the blocked artery and sometimes a stent is put in place to keep it open. The stent can prevent further plaque buildup in that area. For a patient with a STEMI, the goal is to open the artery within 90 minutes of arrival to a facility with a cath lab. If PCI is not available quickly enough, thrombolytic therapy to break up clots within 30 minutes of arrival can be used if the patient meets criteria and has no absolute contraindications. Ninety minutes for PCI. Thirty minutes for thrombolytics. Twelve to 72 hours for PCI in unstable angina or NSTEMI. Those windows matter. They do. And remember the logic: STEMI is an emergency artery-opening problem. UA and NSTEMI still require urgency, but STEMI is the fastest clock in the room. [leaning in] Tiny memory aid: Stable stays the same. Unstable is unpredictable. NSTEMI is No ST elevation but positive enzymes. STEMI is ST up, artery shut. Not perfect poetry, but it sticks. My preceptor version is even shorter: rate, regular, P, PR, QRS, ST, T. Same sequence every time so your brain doesn't skip around. That repetition helps. Let's understand better what each wave or interval means. The first wave, the P wave, is atrial depolarization or contraction. The PR interval is the rate from cardiac impulse through the AV node. Next is that super spike we know as the QRS. The QRS is the ventricle depolarization or contraction. So P- atrium squeezes, AV node fires, then QRS- ventricles squeeze. Next comes the ST segment which gets super important when we talk about heart attacks later. The ST interval is that time between the ventricle squeeze and the relaxation or repolarization. The T wave itself is showing the ventricle repolarizing, which we want to see! A missing or inverted T wave means that ventricle could not fully repolarize or relax which means oxygenated blood is not pumping out to the body like it should. [warmly] I love that image. So let's start with an easy one: sinus bradycardia: slow rate but still normal rhythm. Patients may be asymptomatic, or they may have fatigue, dizziness, shortness of breath, chest pain, near syncope, mental status changes -- basically cues of decreased cardiac output. Nursing actions include monitoring ECG and vital signs, fall precautions if symptomatic, identifying cause, and preparing for treatment. Unstable symptomatic bradycardia gets IV atropine 1 mg, repeated every 3 to 5 minutes up to a total of 3 mg, and if the patient remains unstable, prepare for temporary transcutaneous pacing. And don't forget the simple basics first: do they have a pulse, what is the blood pressure, are they mentating, do they need oxygen, do you have IV access, and can you get help in the room fast? Sinus tachycardia is different because usually the rhythm itself is not the whole story -- it's often a clue to something else. Pain, fever, anxiety, dehydration, infection, stress, medications. Symptoms can include palpitations, dizziness, chest pain, shortness of breath. Right. So with sinus tach, ask why. Treat the underlying cause. Decrease fever or pain, manage anxiety, address dehydration. Medications may include adenosine or beta blockers in certain tachy situations per orders, but the big nursing move is don't just stare at the monitor -- look for the driver. Atrial flutter: atria beat faster than ventricles. The atrial rate can range from 240-400 beats per minute. This is caused by multiple rapid electrical impulses being sent from the atrial too quickly for the AV node to process before the transmission to the ventricles. Overall heart rhythm is regular. P waves are replaced by multiple sawtooth or flutter waves between QRS complexes. Ventricular rate is typically normal 60-100 beats per minute. Patients may have palpitations, hypotension, dizziness, chest discomfort, shortness of breath. Risk factors include recent MI, recent cardiac surgery, and antiarrhythmic medications. Nursing care includes monitoring vital signs and oxygen saturation, giving antiarrhythmics or anticoagulants as ordered, and preparing for cardioversion if needed. Atrial fibrillation is the one students see all the time on exams and in practice. The SA node is not firing properly which causes irregular contractions to the heart. Instead of a nice sawtooth appearance on the EKG strip, it looks like rapid, chaotic, irregular. Irregular rhythm with no organized P waves. The ventricular rate can be normal or fast, and if it's over 100 we call it rapid ventricular response. And the bedside implications are twofold: reduced cardiac efficiency and clot risk. That's why A-fib patients can have palpitations and fatigue, but you're also thinking stroke. When cardiac output is decreased by this chaotic pumping, blood clots can easily form. And we know that blood clots shooting out of the heart and into the blood stream can lead to major complications, including stroke when blood clots travel to the brain. This is why most people with chronic afib are on anticoagulants. Yes -- bleeding precautions if they are anticoagulated, and teach them to report symptoms, take meds as prescribed, avoid stimulants and herbal supplements, and understand why anticoagulation matters. Diagnostics can include TSH, thyroxine, CBC, creatinine, glucose, INR, echocardiogram, and TEE to look for clots in the left atrium. Cardioversion may also be indicated if traditional treatments do not work or the patient becomes unstable. Let's do the scary ones. Ventricular tachycardia: ectopic foci or premature, random electrical take over. The work of the SA node has been taken over and is dangerous because cardiac output drops and it can become ventricular fibrillation. Stable VTach with a pulse might get antidysrhythmic meds or elective cardioversion. However, a pulseless VTach is an extreme emergency! Start CPR, call a code, and start rapid defibrillation. And torsades de pointes is a form of VT associated with long QT. On an EKG strip it looks almost like a twist. This can be caused by electrolyte imbalances, drug toxicity, CNS disorders, heart disease. Can be stable with a pulse or unstable and pulseless. Sustained VT can lead to hypotension, pulmonary edema, decreased cerebral blood flow, or arrest. Now for Ventricular fibrillation: this is definitely a medical emergency because the ventricles are quivering rather than pumping so cardiac output is minimal. The patient is unresponsive, pulseless, apneic. Immediate CPR, rapid defibrillation, ACLS drugs like epinephrine and amiodarone. No dithering. This is not a "let's watch for a minute" rhythm. Asystole: a total absence of ventricular electrical activity. Must assess in more than one lead, because you do not want to call asystole on a loose lead. But if it is real asystole -- unresponsive, pulseless, apneic, CPR and ACLS. Prognosis is poor. And then PEA, which always feels cruel because the monitor gives you electrical activity, but the patient has no pulse. So you don't treat the screen, you treat the patient. Exactly. Pulseless electrical activity means no mechanical output despite electrical rhythm. CPR, epinephrine, and hunt the cause fast. The H's and T's matter: hypovolemia, hypoxia, hypoglycemia, hypothermia, hyper- or hypokalemia, hydrogen ion acidosis, toxins, tamponade, thrombosis MI or PE, tension pneumothorax, trauma. Immediate nursing actions for unstable rhythms are beautifully simple and high-yield: assess pulse and blood pressure, assess airway and breathing, apply oxygen, get IV access, put the patient on continuous monitoring, notify rapid response or call for help, and prepare for atropine, pacing, synchronized cardioversion, defibrillation, CPR, and ACLS as indicated. [crisp] And if you're wondering what's the first thing -- it's not the perfect rhythm name. It's: are they perfusing? Pulse, pressure, mentation. Then act. If I could sit next to every student taking a cardiac exam, I'd write one sentence on the desk: start with ABCs, then perfusion, then rhythm and labs. Because cardiac questions love to tempt you with fancy details before you've answered, "Is this patient stable?" Exactly. Airway, breathing, circulation first. Then ask: is oxygen delivery threatened right now? Chest pain with diaphoresis and hypotension beats a mild lab abnormality every time. Pulseless VT beats a troponin trend question. Altered mental status with bradycardia and low BP beats patient teaching. Here's how I coach people through stems. If you see chest pressure with exertion that resolves with rest or nitro, think stable angina. If it radiates to jaw or arm, comes with dyspnea or diaphoresis, or is happening at rest or getting worse, your concern level rises fast. Then you look for the tie-breakers: ST changes, troponin rise, hemodynamic instability. And if the stem gives you ST elevation in two adjoining leads, do not overthink it. That is STEMI language. Reperfusion. PCI within 90 minutes if possible, thrombolytics within 30 minutes if PCI is not available and there are no contraindications. If it says no ST elevation but troponins are elevated, that's your NSTEMI clue. If pain is new or worsening at rest and biomarkers are negative, unstable angina. Those are such testable distinctions. For dysrhythmias, NCLEX often hides the answer in hemodynamic words: dizzy, confused, hypotensive, chest pain, short of breath, decreased urine output, syncope, unresponsive, pulseless. Those words matter more than whether you personally think the strip looks dramatic. Yep. Stable rhythm problem versus unstable patient problem. If the patient with A-fib is chatting, perfusing, and just needs chronic management, that's a different urgency than A-fib with hypotension and chest pain. Same rhythm name, very different priority. Teaching priorities are also huge. Medication adherence first. Antihypertensives only work if taken, and side effects like orthostatic hypotension, frequent voiding, dry mouth, or sexual dysfunction can cause nonadherence. Patients should report side effects so the regimen can be adjusted rather than silently stopped. I appreciate that one because in real life, people don't say, "I am noncompliant." They say nothing, and then two months later the pressure is 178 over 96 because the medication made them feel awful. Nitroglycerin teaching: use it as prescribed for angina, understand that stable angina should improve with rest or nitro, and know when symptoms have crossed into emergency territory -- pain at rest, pain lasting longer, pain not relieved as expected, associated diaphoresis, dyspnea, or worsening symptoms. Bleeding precautions with anticoagulants and antiplatelets because of thrombocytopenia: fall prevention, soft toothbrush, careful shaving, report bleeding, and understand why they're on the med. Blood thinners after stent placement is not optional vibes -- it's prevention of stent thrombosis. Lifestyle teaching has to be specific enough to act on: smoking cessation, heart-healthy diet, maintain healthy weight, physical activity, quality sleep, sodium reduction for hypertension, moderation of alcohol, and follow-up visits. Even a 1 kilogram weight loss can decrease systolic pressure by about 1 mm Hg. That 1 kilogram to 1 mm Hg relationship is wonderfully concrete. It gives patients something measurable, not just "you should probably lose some weight." And older adults need careful teaching too: orthostatic risk, slower dose changes, watch NSAID use because it can worsen blood pressure control and heart failure risk, and remember white coat hypertension is more common. My favorite NCLEX shortcut is this: if the answer restores perfusion faster, it usually wins. Apply oxygen. Get the ECG. Give the aspirin if indicated. Start the IV. Call the rapid response for the unstable rhythm. Prepare for reperfusion. Protect the brain and the myocardium first; charting and long education can wait five minutes. [reflective] That's such a good way to frame it -- restore perfusion faster. Because under all the terminology, all the strips, all the meds, the body is still asking the same simple question we started with: are you getting oxygen to the tissues or not? And when students really get that, the cardiac chapter stops feeling like memorizing random disasters. It starts feeling organized. Organized, but never casual. Because the patient who looks "not that bad" at 10:02 can become the emergency at 10:12. [softly] Which is why we pay attention early. All right -- that's the heartbeat of it. I know that was long and a lot of information, but I hope it helped to paint the picture of hypertension and atherosclerosis. And how those can lead to coronary artery disease and acute coronary syndrome, which can consist of stable or unstable angina, NSTEMI, or worst case- STEMI. Do not stress so much over perfecting EKG readings at this point. Be able to recognize basic rhythms, what they mean, and how to treat. As you get practice, it will become easier. Until next time, take care of your heart!
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