This episode of Think Like a Nurse, created by Brooke Wallace, a 20-year ICU nurse, organ transplant coordinator, clinical instructor, and published author, walks listeners through a high-yield rapid review of cardiac pathophysiology for the NCLEX. Instead of drowning in textbook detail, the conversation focuses on the most testable conditions: acute coronary syndromes, heart failure and cardiogenic shock, and pericarditis and infective endocarditis. You’ll learn how to recognize myocardial infarction vs angina, differentiate stable, unstable, and Prinzmetal angina, compare left-sided and right-sided heart failure, identify the signs of cardiogenic shock, and spot classic findings of pericarditis and infective endocarditis. The hosts repeatedly pull out NCLEX priorities, such as “time is muscle,” treating unstable angina like an MI, using daily weights as the best noninvasive fluid status monitor, and remembering critical medication rules and contraindications that protect patients from harm.
Acute coronary syndromes (ACS) – blocked arteries and myocardial infarction
Pump failure – heart failure and cardiogenic shock
Infection and inflammation – pericarditis and infective endocarditis
Constant NCLEX theme:
Assessment before action
Time is muscle in ACS
Fluid status is king in heart failure and shock
Core pathophysiology
Coronary artery becomes blocked.
Downstream heart muscle becomes ischemic and, if prolonged, becomes necrotic.
NCLEX hallmark MI features
Chest pain > 20 minutes, not relieved by rest or nitroglycerin.
Pain plus systemic signs: sweating, nausea, shortness of breath, “impending doom.”
Troponin I or T elevated – most specific cardiac biomarker.
ST elevation on ECG = STEMI → true emergency.
MONA (bedside actions while waiting for reperfusion)
M – Morphine: relieves pain and decreases preload, lowering workload on the heart.
O – Oxygen: maintain oxygen saturation ideally above 94.
N – Nitroglycerin: vasodilates coronary arteries; check blood pressure first and avoid if hypotensive.
A – Aspirin: 162–325, chewed for faster absorption; prevents platelet clumping and clot growth.
Reperfusion priorities
PCI (percutaneous coronary intervention): goal is door-to-balloon time within 90 minutes.
If PCI is not possible within about 120 minutes, use fibrinolytics (clot busters).
Post-MI complications to watch
Ventricular dysrhythmias: premature ventricular contractions, runs of V-tack, or ventricular fibrillation needing immediate defibrillation.
Cardiogenic shock.
Papillary muscle rupture leading to acute severe mitral regurgitation.
Shared concept
Chest pain occurs when oxygen demand exceeds oxygen supply, usually due to coronary artery disease.
Stable angina
Trigger: predictable exertion or emotional stress.
Duration: less than 20 minutes.
Relief: rest or nitroglycerin.
Pattern matters: “I walk upstairs, get pain, sit, and it goes away.”
Unstable angina (NCLEX favorite)
Represents a change:
Occurs at rest or with increasing frequency, duration, or intensity.
NCLEX rule:
Treat unstable angina as acute coronary syndrome.
Start MONA, continuous monitoring, and assume MI until proven otherwise.
Prinzmetal (variant) angina
Caused by coronary artery spasm, not always a fixed blockage.
Often occurs at rest or at night.
Typically responds to calcium channel blockers like diltiazem; nitroglycerin can also help.
Core concept
Heart cannot pump effectively → fluid backs up in the lungs or in the body.
Left-sided heart failure – “Think lungs”
Fluid backs up into the pulmonary circulation.
Key findings:
Shortness of breath.
Crackles on auscultation.
Orthopnea – difficulty breathing when lying flat.
Paroxysmal nocturnal dyspnea – waking suddenly gasping for air.
Right-sided heart failure – “Think body”
Fluid backs up into systemic circulation.
Key findings:
Jugular vein distension.
Peripheral edema – swelling in legs and ankles.
Hepatomegaly – enlarged liver.
Ascites – fluid in the abdomen.
Best noninvasive fluid status monitor
Daily weights:
Same time, same scale, same clothing.
Report gain of about 2–3 pounds in one day or 5 pounds in one week.
Common heart failure medications
ACE inhibitors (example: lisinopril) – decrease afterload.
Beta-blockers (example: carvedilol, metoprolol) – reduce heart rate and workload, protect the heart long term.
Digoxin – increases contractility; watch closely for digoxin toxicity (nausea, visual changes like halos, slow heart rate).
Diuretics:
Loop diuretics such as furosemide remove excess fluid.
Spironolactone is potassium-sparing and also helps with fluid.
Key lab
BNP (brain natriuretic peptide):
Elevated BNP indicates worsening heart failure and increased cardiac stretch.
Patient teaching
Low-sodium diet, typically less than 2 grams a day.
Follow fluid restriction if prescribed.
Understand warning signs: rapid weight gain, increasing shortness of breath, swelling.
When it happens
Frequently a complication of a large MI.
Heart muscle is so damaged it cannot maintain adequate cardiac output.
Key assessment features
Profound hypotension – very low systolic blood pressure.
Decreased urine output – typically less than 30 per hour, showing poor kidney perfusion.
Cool, clammy skin.
Weak, thready pulses.
Altered mental status – confusion, lethargy.
Medications used
Dopamine – increases blood pressure and cardiac output at certain doses.
Dobutamine – increases contractility.
Norepinephrine – go-to vasopressor for severe hypotension.
Mechanical support
Intra-aortic balloon pump (IABP):
Inflates and deflates in sync with the heart.
Decreases workload on the left ventricle and improves coronary perfusion.
Primary goal
Maintain vital organ perfusion.
Target: mean arterial pressure (MAP) above 65 to protect organs like brain and kidneys.
Pathophysiology
Inflammation of the pericardium, often after viral illness, kidney failure, or MI.
Pain pattern (NCLEX gold)
Sharp, pleuritic chest pain:
Worse with deep breathing, coughing, or lying flat.
Improves when the patient sits up and leans forward – classic positional relief.
Assessment findings
Pericardial friction rub – scratchy, leather-like sound.
ECG: diffuse ST elevation across many leads, sometimes with PR depression.
Treatment
High-dose NSAIDs (example: ibuprofen).
Colchicine often added to reduce recurrence.
Critical NCLEX “do not”
Do NOT give anticoagulants (no heparin, no warfarin) in pericarditis.
Risk: bleeding into the pericardial sac → cardiac tamponade.
Cardiac tamponade – life-threatening complication
Beck’s triad:
Low blood pressure.
Muffled or distant heart sounds.
Jugular vein distension.
Pulsus paradoxus:
Significant drop in systolic blood pressure with inspiration.
Requires immediate pericardiocentesis to drain fluid and relieve pressure.
Pathophysiology
Infection of the endocardium and valves, usually bacterial (strep or staph).
Vegetations can break off and cause emboli.
NCLEX hallmark signs
Persistent fever.
New or changing heart murmur – suggests valve damage.
Embolic phenomena (high-yield “weird” signs)
Janeway lesions – small, painless spots on palms and soles.
Osler nodes – small, painful nodules on fingers or toes.
Roth spots – retinal hemorrhages.
Splinter hemorrhages – thin, dark lines under fingernails.
Management
Prolonged IV antibiotics, often 4–6 weeks or longer (examples: vancomycin, gentamicin, depending on organism).
Critical first step:
Obtain blood cultures before starting antibiotics (usually three sets from different sites).
Use echocardiography:
Start with transthoracic, escalate to transesophageal if needed.
Nursing priorities
Monitor for new embolic events – stroke symptoms, splenic pain.
Watch for worsening heart failure from valve destruction.
Educate high-risk patients about prophylactic antibiotics before dental procedures.
Assessment Before Action
Always gather data first: vital signs, pain description, lung sounds, ECG changes, urine output, mental status.
Use SBAR to communicate: Situation, Background, Assessment, Recommendation.
Fluid Status Is King
Especially critical in heart failure and shock.
Daily weights are your best noninvasive monitor:
About 2–3 pounds gain in a day or 5 pounds in a week = red flag.
Know Your Critical Medication Rules
MONA is for acute coronary syndrome, not stable angina.
Never give anticoagulants in pericarditis because of tamponade risk.
Treat unstable angina like an MI until ruled out.
Watch for digoxin toxicity and be intentional with vasopressors and inotropes.
Connect the Dots
One cardiac problem often leads to another:
Large MI → cardiogenic shock.
MI → later pericarditis.
Valve infection → heart failure or stroke.
Thinking like a nurse means seeing relationships between conditions, not just memorizing lists.
Welcome to Think Like a Nurse. This is the show created by Brooke Wallace. She's a 20-year ICU nurse, organ transplant coordinator, clinical instructor, and a published author, too. Mhm. Our mission really is simple. We take these complex nursing topics, things that can feel overwhelming, and we try to make them easier for you to understand, especially when you're gearing up for the ENCLEX RN. Absolutely. And you can always find more resources over at think like nurse.org to help you along the way.
So, today, what are we tackling? Today, we are doing kind of a college sprint, a rapid review through some critical cardiac pathophysiology. Okay? Instead of getting bogged down in, you know, massive textbook chapters, we're zeroing in on the absolute must know facts, the key assessments, and those crucial interventions you need for the exam, taking the noise. Exactly. Trying to avoid that information overload. We've sort of chunked it into three main areas. Acute coronary syndromes, pump failure, and then infection or inflammation issues.
That sounds like a really smart way to organize it. Maximize retention, right? That's the goal. Okay, let's dive right in then. Highest stakes first. Acute coronary syndromes. The big phrase here is always time is muscle. Couldn't be more true. It really sets the urgency. It absolutely does. And when we talk ACS, the immediate emergency is usually a myioardial inffection. You know, an MI, a heart attack, right? Essentially, a coronary artery gets blocked, oluded, and that starves the heart muscle downstream of oxygen. That leads to eskeeia and And if it goes on long enough, actual tissue death, necrosis,
and the faster you fix that blockage, the more heart muscle you save. Simple as that. So for the inlex, how do they expect us to spot this? What separates like bad indigestion from a true MI? What are those hallmark signs? Okay, good question. The key differentiators are chest pain that lasts longer than 20 minutes. That duration is important. And critically, it's pain that isn't relieved by rest or by taking nitroglycerin. Those are huge red flags. Okay, pain not going away. Diagnostics what confirms it
diagnostically the gold standard the most specific cardiac biioarker is looking for an elevated tropponin level either tropponin I or tropponent t right and if you see st segment elevation on the EKG that's your STEMI ST elevation MI that is a code level emergency okay STEMI confirmed before they get whisked off to the kath lab what are the immediate bedside steps there's that pneummonic right mia yes M&A super important, but it's not just a checklist. It's um it's a sequence with purpose.
Okay, break it down for us. M M is morphine. Yes, it helps with the intense pain, which is vital, but clinically, it also does something else really important. It decreases preload, uh reducing the workload on the heart. Exactly. It kind of calms everything down, takes some pressure off that struggling heart muscle right now. O is for oxygen. Pretty straightforward. We want to keep their oxygen saturation ideally above 94%. Maximize oxygen delivery to whatever tissue is still getting perused.
Makes sense. N N is nitroglycerin. It's a vasoddilator. Helps open up those coronary arteries. But big caution here, you must check their blood pressure first, right? Can't bottom them out. Definitely not. If they're already hypotensive, nitro could make things much worse. So only if BP is stable. Good point. And finally, A. A is for aspirin, specifically 162 to 325 millig. And the key here is that it needs to be chewed. Why chewed? Faster absorption. Exactly. Chewing ensures rapid absorption through the mucous membranes in the mouth. Its job is to prevent platelets from sticking together to stop that clot from getting any bigger while we're waiting for definitive treatment like PCI.
So M&A buys us critical time. Which brings us to reprofusion. You mentioned PCI. That door to balloon time is crucial, isn't it? Hugely crucial. The goal is perccutaneous coronary intervention. Getting that block artery open with a balloon. Maybe placing a stent ideally within 90 minutes of the patient arriving at the hospital door. 90 minutes. Wow. What if PCI is available quickly? Yeah, not every hospital has a calf lab available to a first seven. If PCI can't be done within about 120 minutes, then the alternative is fibiberolytics, clot busting drugs.
Okay. Now, while all this is happening, that injured heart muscle is pretty unstable electrically speaking. What complications like arrhythmias should we be watching for very closely? Oh, definitely. PostMI, the heart is irritable. You have to be vigilant for ventricular dysriythmias things like PVC's runs of VTach or the worst case scenario VIB which needs immediate defibrillation immediately no delay also watch for signs of pump failure leading to cardiogenic shock or um a really catastrophic mechanical problem like a papillary muscle rupture
would cause what? So severe mitro valve regurgitation a real mess okay that covers the full-blown MI but the ENLEX loves to test the difference between that and angina pectorus that's chest pain from oxygen demand exceeding supply Right? Usually due to underlying coronary artery disease. Correct. It's like the heart is complaining. It's not getting enough oxygen for the work it's doing. So, how do we tell the types apart? Let's start with stable angina. Stable angina has a predictable pattern. It's typically triggered by physical exertion or sometimes emotional stress. Critically, it lasts less than 20 minutes and it's relieved by rest or taking nitroglycerin.
So, they walk upstairs, get pain, sit down, pain goes away. That pattern. Exactly. That predictability. is key. Okay. Then what about unstable anggina? This one feels like the tricky one. It is tricky because it represents a change. Unstable angina either occurs at rest without a clear trigger or it happens with increasing frequency, duration or intensity. Maybe pain that used to only happen after walking two blocks now happens after half a block. So what's the enclelex takeaway for unstable angina? How do we approach it?
The absolute crucial point, treat unstable angina as part of acute coronary syndrome. That means you initiate the NA protocol. Assume it's an MI until proven otherwise. Don't wait. Treat it aggressively upfront. Precisely. Because clinically that plaque might have ruptured. A clot might be forming. It's potentially an evolving MI. Okay. And the last type, prince metals or variant anggina. Yeah. Prince metals is different. It's caused by a spasm in the coronary artery, not necessarily a fixed blockage. It often happens weirdly at rest, frequently at night.
And the treatment is different, too. Yes. Since it's a spasm. It often responds well to calcium channel blockers like diliasm which help relax that smooth muscle in the artery wall. Nitroglycerin can help too but calcium channel blockers are sort of the characteristic treatment. All right, very clear distinctions there. Let's shift gears now. Moving away from the plumbing blockages to problems with the engine itself. Our second bucket, the pump problem, heart failure and cardiogenic shock. Right? So heart failure or HF is fundamentally the heart not being able to pump effectively enough to meet the body's demands. This leads to fluid backing up either in the lungs or in the rest of the body.
And the enclelex often wants us to differentiate leftsided versus right-sided failure. Let's start with left. If the left ventricle fails, where does the fluid go? It backs up into the pulmonary circulation into the lungs. So, you get pulmonary congestion. Meaning what signs and symptoms? Shortness of breath or dysnia. You'll hear crackles on oscultation. Orthopia, difficulty breathing when lying flat. And that classic Enclelex favorite Peroxismal nocturnal dismia PND waking up suddenly gasping for air.
Exactly. It's terrifying for the patient. Okay. So that's leftsided. Think lungs. What about right-sided failure? If the right ventricle fails, the backup is in the systemic circulation before the blood even gets to the lungs. So signs we'd see are more bodywide. Correct. Things like jugular vein distension, JVD in the neck, peripheral edema, so swelling in the legs and ankles, hippatomegali, an enlarged liver and sometimes acites which is fluid accumulation in the abdomen. Okay, lots of fluid issues here. You mentioned tracking fluid. What's the single best most practical way for a nurse to monitor fluid status dayto-day?
Without a doubt, it's daily weights. Same time, same scale, same amount of clothing every single day. And what kind of weight gain is the alarm bell? You need to know these numbers for the Enclelex. Report any gain greater than 2 to three lbs in just one day or a gain of more than 5 lbs in one week. Those specific numbers, those rapid gain s scream fluid retention and worsening heart failure. It needs intervention. So managing HF involves meds. It's often a combination strategy, right? Targeting different problems.
Definitely. It's about reducing the heart's workload and maybe improving its pumping strength. So we often use AC inhibitors like listen opal. They reduce afterload the resistance the heart pumps against. Makes the job easier, right? Then beta blockers like carvidol or metoprolol. They slow the heart rate and reduce the overall workload, kind of protect the heart long term. Okay. What about strengthening the pump? That's where dioxin sometimes comes in. It increases contractility makes the squeeze stronger, but big, but you have to watch very carefully for dioxin toxicity. Narrow therapeutic window,
right? The halos, nausea, brady cardia, all those signs. And of course, diuretics are key, like fioamide, a loop diuretic, or maybe spironolactone, which is potassium bearing to help get rid of that excess fluid. Got it. Is there a lab test that specifically It tells us HF is getting worse. Yes, BNP, brain naturetic peptide. When the heart muscle is stretched and stressed like in worsening HF, it releases more BNP. So, an elevated BNP level is a clear indicator of exacerbation which underlines the importance of patient teaching, right? Low sodium diet
absolutely crucial. Limiting sodium to less than 2 grams per day is standard and often fluid restrictions are necessary too. Patients really need to understand and follow those. Okay. From chronic HS Let's talk about the acute life-threatening version of pump failure. Cardiogenic shock often follows a big MI, you said. Yes. It's a common and devastating complication of a large MI. Basically, the heart muscle is so damaged, it simply cannot generate enough cardiac output to peruse the vital organs. It's catastrophic pump failure.
And the assessment findings are pretty traumatic, I imagine. What's the key triad we look for? The classic triad indicating shock. One, profound hypotension systolic blood pressure typically less than 90 milli. Two, signs of poor organ profusion, especially decreased urine output, usually less than 30 millmer per hour. That tells you the kidneys aren't getting enough blood flow. Kidney shutting down. Okay. And the third third is the physical signs of poor profusion. Cool, clammy skin, weak or thready pulses, altered mental status, confusion, lethargy. The body is shutting down.
Interventions must be aggressive then focused on supporting that blood pressure. and profusion extremely aggressive. We use potent medications vasopressors and inert tropes things like dopamine debutamine to try and boost contractility and cardiac output and norepinephrane often the go-to for severe hypotension to clamp down blood vessels and raise pressure. Any mechanical support options? Sometimes yes. An intraortic balloon pump or IABP might be used. It's a device inserted into the aorta that inflates and deflates in sync with the heartbeat to help decrease the workload on the left ventricle and improve coronary artery profusion. And the ultimate goal with all this,
the immediate goal is to maintain vital organ profusion. A key target is keeping the mean arterial pressure, the map, above 65 millg. That's generally considered the minimum needed to keep organs like the brain and kidneys happy. MAP above 65. Got it. Okay, that covers pump failure. Let's move to our final stack. Infection and inflammation affecting the heart. Starting with paricarditis. Paricarditis, inflammation of the paricardium, that sack surrounding the heart. And the pain is key here, right? How does it differ from MI pain?
Yes. The pain quality and its modifiers are classic anklelex material. It's typically described as sharp puritic chest pain, meaning it worsens with deep breathing or coughing or when lying flat. And the big clue, the pain improves significantly when the patient leans forward. Sitting up and leaning over a bedside table often provides relief. That positional change is highly characteristic. Anything else on assessment? You might oscultate a paricardial friction rub. Sounds like scratchy leather. And the EKG often shows diffuse ST segment elevation across multiple leads unlike the more localized changes in an MI sometimes PR depression too.
How do we treat the inflammation usually with anti-inflammatories highdosese NSAIDs like ibuprofen are first line cultine is often added as well okay now what's the absolute critical don't with paricarditis the good medication contraindication this is vital do not give anti-coagulants no hepin no warrin why not Because the inflamed paricardium is already prone to issues. Anti-coagulation dramatically increases the risk of bleeding into that paricardial sack bleed to cardiac tamponate. A potentially fatal complication where fluid accumulates rapidly in the sack compressing the heart and preventing it from filling properly.
Tampenade that requires immediate action. What are the signs? Beck's triad. Exactly. Beck's triad for tamponade. One, hypotension, low blood pressure. Two, muffled or distant heart sounds because the fluid is in olating the heart and three jugular vein distension JBD because the blood can't get into the compressed right side of the heart easily. Anything else? Pulsus paradoxis. Yes, that's another important sign. Pulsus paradoxis is an exaggerated drop in systolic blood pressure typically more than 10 millh during inspiration. It reflects the impaired filling.
And if you see beex triad or suspect pamp it's an emergency requires immediate paricardioentesis inserting a needle into the paricardial sack to drain the excess fluid and relieve the pressure on the heart. Wow. Okay. Critical complication. Let's finish with infective endocarditis. Infection inside the heart lining. Right. Usually valves. Correct. It's an infection typically bacterial like strep or staff affecting the endocardium, the inner lining, and especially the heart valves. What's the main danger here?
The biggest concern is the risk of embleization. The infection forms vegetations, clumps of bacteria and debris on the valves. Pieces of these vegetations can break off and travel through the bloodstream becoming emblei. Okay. So, what are the key signs for enclelex? The most common findings are persistent fever and importantly a new or changing heart murmur that suggests valve damage from the infection. But there are also those really unique almost weird signs related to the emblei, aren't there?
Yes, the embolic phenomena. These are often tested because they're so specific things like Janeway lesions, small painless spots usually on the palms or soles. Contrast those with osler's nodes. small painful nodules typically on the fingertips or toes. Painless versus painful. Okay. Right. You might also see Roth spot, small hemorrhages in the retina visible on eye exam and splinter hemorrhages which look like tiny dark lines under the fingernails. All clues that infected bits are showering the body.
So, how do we manage endocarditis? It's all about the infection primarily. Yes. It requires prolonged courses of IV antibiotics often for four to six weeks, sometimes even longer. Potent antibiotics like venkcom Isin or gentamison are common depending on the bacteria. And what's the absolute first nursing step before starting those antibiotics? This is crucial. You must obtain blood cultures first. Typically three sets drawn from different sites spaced out over time. You need to identify the specific organism causing the infection to guide antibiotic choice.
Get the cultures before the drugs. Makes sense. Absolutely. Then ongoing monitoring is key watch for signs of new emolic events like a stroke if an embolis goes to the brain or signs of worsening heart failure. if the valve damage becomes severe. Wow. Okay, we've covered a lot of ground ACS, pump failure, inflammation. That was a really dense high yield review. Let's try to synthesize. What are maybe the top three crosscutting clinical priorities that kind of apply across all these cardiac conditions for ENLEX prep?
Okay, three big takeaways. First, assessment always comes before action. Always. Gather your data, vital signs, patient report, lung sounds, EKG changes before you jump to intervene or call the provider. Use a structure to approach like SBIR when you do communicate assessment first. Got it. Second, fluid status is king in so many cardiac issues. Heart failure shock. Remember, daily weight is your best friend for non-invasive monitoring. Know those critical weight gain numbers. 2 three lbs in a day, 5 lbs in a week. Act on those.
Daily weights. Yeah. Crucial. Okay. And third, third, know your critical medication rules and contraindications. Cold. Ma is for ACS, not stable angina. Absolutely. Never give anti-coagulants for paricarditis. You risk tamponade. And always, always treat unstable angina like it's an MI until definitively ruled out. Don't wait. MOA for ACS. No anti-coag for paricarditis. Unstable angina equals MI precautions. Perfect summary. Those are huge safety points. So thinking about all this for you, the listener,
what's the final thought? How does this all connect? Well, it's important to realize that while we discuss these conditions separately, a blockage here, a weak pump there, an infection And over here the cardiac system is deeply interconnected, right? So one problem like a big MI often sets the stage for another life-threatening issue like cardiogenic shock or maybe pericarditis develops later as an inflammatory response. It's rarely just one thing in isolation. So the key is connecting those dots. Seeing the relationship.
Exactly. Understanding how one cardiac issue can lead to or complicate another. That's really moving towards thinking like a nurse. Seeing the whole picture. That's a great perspective. Keep connecting those dots. You can definitely do it. Well, thank you. so much for joining us for this really valuable conversation today. We hope this helps you feel more confident. Hope so too. We invite you to check back in for more essential talks each week. And remember, you can always find more resources and support at think like a nurse.org.
Keep up the great work. We'll talk to you next time on Think Like a Nurse.