In this episode of Think Like a Nurse, we will walk you step by step through a full cardiac assessment, from room setup to bedside prioritization. You’ll connect what you hear in your stethoscope and see in your assessment with what’s happening inside the heart—electrical, pump, and perfusion. Perfect for nursing students, new grads, and NCLEX prep, this conversation breaks down vital signs, heart sounds, murmurs, jugular venous distention, peripheral pulses, edema, and key cardiac meds like beta blockers, ACE inhibitors, and loop diuretics. You’ll also practice thinking like a nurse by walking through clinical patterns that scream shock, acute heart failure, or arterial occlusion so you know exactly who to see first and what to do next.
Quiet, warm, well-lit environment is non-negotiable so you don’t miss subtle sounds.
Standard position: supine with head of bed at about 30–45 degrees for blood pressure and jugular vein assessment.
Use left lateral decubitus to bring the apex closer to the chest wall for a faint apical pulse or mitral murmur.
Follow the systematic framework IPPA: inspection, palpation, percussion, auscultation to stay organized.
Normal heart rate is about 60–100; sustained under 50 or over 120 is a call-the-provider situation.
Blood pressure target is under 120 over 80; hypotension under about 90 over 60 is concerning, especially with symptoms.
Pulse pressure = systolic minus diastolic:
Narrow pulse pressure (less than about 25) suggests low stroke volume and possible shock or significant fluid loss.
Wide pulse pressure (greater than about 40–50) can point to aortic regurgitation or high-output states like fever.
Metoprolol (beta blocker)
Lowers heart rate and blood pressure.
Watch for bradycardia, hypotension, dizziness.
Lisinopril (ACE inhibitor)
First-dose effect: risk of sudden hypotension in the first hours.
Monitor blood pressure closely, especially at initiation.
Furosemide (Lasix, loop diuretic)
Rapidly removes fluid, lowering preload in fluid overload and heart failure.
Monitor blood pressure, heart rate, hydration status, and symptoms of low volume.
S1 (“lub”)
Closure of mitral and tricuspid valves at the start of systole.
Loudest at the apex.
S2 (“dub”)
Closure of aortic and pulmonic valves at the start of diastole.
Best heard at the base of the heart; can split slightly with inspiration (normal).
S3 (“Kentucky”)
Low-pitched, early diastolic sound after S2.
Heard best with bell at the apex, often in left lateral position.
Classic for volume overload and acute heart failure.
S4 (“Tennessee”)
Low-pitched, late diastolic sound right before S1.
Reflects a stiff, non-compliant ventricle.
Seen in long-standing hypertension, ventricular hypertrophy, aortic stenosis.
Aortic – 2nd intercostal space, right sternal border.
Pulmonic – 2nd intercostal space, left sternal border.
Erb’s point – 3rd intercostal space, left sternal border.
Tricuspid – 4th intercostal space, left sternal border.
Mitral / Apical – 5th intercostal space, mid-clavicular line (PMI).
Technique:
Use diaphragm first for S1, S2 and higher-pitched sounds.
Use bell lightly for low-pitched S3, S4 and some murmurs.
Move in a consistent pattern (base-to-apex or apex-to-base) so you don’t miss a spot.
Murmurs = turbulent blood flow, graded I to VI by intensity.
Grade IV and above: you can feel a palpable thrill (vibration) on the chest wall.
Systolic murmurs occur between S1 and S2; two must-know examples:
Mitral regurgitation:
Systolic murmur at the apex.
Often radiates to the axilla.
Aortic stenosis:
Harsh systolic murmur at 2nd right intercostal space,
Radiates to the carotid; classic exam description.
Keep head of bed at about 30–45 degrees.
Measure vertical height of venous pulsation above the sternal angle.
Normal JVD is 3 centimeters or less above the sternal angle.
More than 3 centimeters suggests elevated right atrial pressure and:
Right-sided heart failure,
Severe fluid overload,
Or cardiac tamponade (fluid compressing the heart).
For volume overload with JVD, think loop diuretics to decrease preload.
Peripheral pulses grading:
0 – absent.
1+ – weak, thready.
2+ – normal.
3+ – full, strong.
4+ – bounding.
Always compare bilaterally: radial, dorsalis pedis, posterior tibial, etc.
Absent pedal pulses suggest peripheral artery disease or acute arterial occlusion.
Bounding pulses can suggest aortic regurgitation, fever, or fluid overload.
Bruits (whooshing over carotid or femoral): think narrowing or blockage in that artery.
Capillary refill:
Normal: color returns in under 2 seconds.
Delayed refill suggests poor peripheral perfusion (shock, severe dehydration, advanced P.A.D.).
Pitting edema grading:
1+ – slight pit, disappears quickly.
2+ – deeper, gone in about 10–15 seconds.
3+ – deep, may last around a minute.
4+ – very deep, can last 2–3 minutes or more.
Location clues:
Bilateral leg or sacral edema → think systemic causes (heart failure, kidney or liver disease).
Unilateral edema → think DVT, lymph obstruction, or local injury.
Spironolactone: potassium-sparing diuretic used in chronic heart failure or low-protein edema.
Tachycardia (over 100): look for pain, fever, dehydration, bleeding or shock.
Bradycardia (under 60): check meds like beta blockers, digoxin, calcium-channel blockers and evaluate for heart block.
Atrial fibrillation: irregular rhythm with no clear P waves.
Check ventricular rate first.
Evaluate anticoagulation status due to high stroke risk.
ST-elevation myocardial infarction (stemi):
ST elevation plus symptoms = acute heart attack.
Time is muscle: activate cath lab, and anticipate morphine, oxygen, nitroglycerin, aspirin per protocol.
These assessment combinations should trigger immediate concern:
Falling blood pressure + rising heart rate
Hypotension plus tachycardia → suspect shock until proven otherwise.
New S3 + JVD + crackles in lungs
Classic for acute decompensated heart failure and severe fluid overload.
Priority: diuretics, oxygen, monitoring; notify provider quickly.
Absent pulses + cool, pale limb
Think acute arterial occlusion – vascular emergency.
Limb-threatening; requires immediate intervention.
CNA / tech can:
Measure and report vital signs,
Report objective changes (new swelling, shortness of breath).
RN must:
Perform and interpret cardiac assessment,
Auscultate heart sounds and interpret murmur significance,
Interpret ECG changes, JVD, edema patterns,
Administer IV cardiac meds and adjust care based on findings.
Daily weights:
Same time, same scale, similar clothing.
Report gain of 2–3 pounds in a day or about 5 in a week.
Low-sodium diet (commonly under two grams per day) unless otherwise directed.
Medication adherence:
Understand why they take each med.
Know key side effects (for example, taking carvedilol with food to help tolerance and absorption).
A patient presents with shortness of breath, swollen ankles, blood pressure 98 over 60, heart rate 112. You note JVD at 5 centimeters, bilateral crackles, and a new S3 heart sound. What is the nurse’s first action?
Priority: Notify the provider and prepare to give IV furosemide.
Rationale: This pattern is acute decompensated heart failure with low perfusion and severe fluid overload. Reducing preload quickly is critical to prevent further decompensation.
Speaker 1: Welcome to Think Like a Nurse. We're all about helping you build that critical thinking muscle. Really taking your clinical skills to the next level.
Speaker 2: That's right.
Speaker 1: And today uh we are diving deep into something absolutely fundamental.
Speaker 2: Yeah.
Speaker 1: Mastering cardiac assessment.
Speaker 2: High stakes stuff.
Speaker 1: Absolutely. And this show, Think Like a Nurse, it's well, it's built from the expertise of Brooke Wallace. She's got 20 years in ICU. She's been an organ transplant coordinator, clinical instructor, author, just incredible experience.
Speaker 2: Yeah, amazing background.
Speaker 1: And we're here to take all that knowledge, all those complex cardiovascular concepts you need to know and really break them down. So, our goal today is pretty straightforward. If you're prepping for the ENLEX or honestly, even if you're practicing and just want a solid refresher, we're tackling cardiac assessment.
Speaker 2: It means spotting things early, right? Like heart failure brewing or an MI.
Speaker 1: Exactly. Giving you that clarity, the um the system, and really the prioritization skills so you can recognize as what's truly life-threatening because cardiac assessment fundamentally it's about connecting the dots, isn't it? The electrical side, the pump itself, the hemodynamics.
Speaker 2: It's a systematic evaluation really designed to catch those subtle signs of trouble before things get well bad.
Speaker 1: Okay, let's jump right in then. We're going to walk through the core components basically step by step based on solid clinical practice.
Speaker 2: Sounds good.
Speaker 1: And just a reminder for everyone listening, you can always find more resources over at think like nurse.org.
Speaker 2: Definitely check that out.
Speaker 1: Right. First things first, you can't do a good assessment in a chaotic space.
Speaker 2: Seems obvious, but the sources really stress this. Preparation is foundational.
Speaker 1: It really is. You need a quiet place. Warm, good lighting.
Speaker 2: That quiet part, non-negotiable, right? If you miss a subtle sound,
Speaker 1: you miss a crucial clue. Absolutely. And beyond the environment, patient positioning is well, it's central for the standard checks. Heart sounds, BP, JVD. You want patient supine head of the bed up about 30 to 45°.
Speaker 2: Okay, that slight elevation that's key for seeing the jugular veins properly, isn't it?
Speaker 1: Precisely helps estimate that central venus pressure. But there's a key exception for those really faint sounds, those tricky ones. What position do we absolutely need?
Speaker 2: Uh the left lateral decubitus,
Speaker 1: rolling them onto their left side. Bingo. That position is critical if you want to really nail down the apical pulse or if you're listening for say a faint mitro murmur. It just brings the apex of the heart closer to the chest wall. Makes things easier to hear.
Speaker 2: Makes sense. Okay. So, they're positioned right now. We need a system. The framework is IPA, inspection, palpation, percussion, oscultation.
Speaker 1: Right.
Speaker 2: But hang on. For the admin, we usually do inspection, oscultation, then percussion and palpation. We flip it to avoid messing with bowel sounds before listening. Why stick with IPA for the heart?
Speaker 1: Good question. We stick with IPA for the cardiac assessment primarily to keep it organized. You want to inspect First look for symmetry, any visible lifts or heaves. Then you palpate, feel for thrills, those vibrations, or locate the apical impulse. You do all that before you put the stethoscope on. Percussion, admittedly, it's less commonly emphasized at the bedside for routine cardiac checks compared to say the lungs. But keeping that IPA order ensures you've systematically checked the physical signs first before diving into the listening part, the oscultation.
Speaker 2: All right, moving on from setup to like the first alert system. Yeah, vital signs. These ranges, you just got a known cold.
Speaker 1: They're your immediate red flags. Starting with heart rate, normal is typically 60 to 100, and you should be checking that at the apical pulse for a full minute if it's irregular, right? But the critical numbers, the ones you call about immediately, a sustained rate under 50 or pushing over 120 and super important, any new irregular rhythm like sudden onset aphib, that's a big deal.
Speaker 2: Definitely. Okay. Blood pressure target's pretty clear. Yeah. Less than 120 over 80. Yep. Hypertension is generally defined as over 130 80. And hypotension, the number that really makes you worry is anything consistently under 90/60 systolic. Got it.
Speaker 1: But let's push beyond just those two numbers. We need to talk about pulse pressure. That's the difference, a gap between the systolic and the diastolic.
Speaker 2: Ah, okay. I sometimes get mixed up on the implications. Why is a narrowed pulse pressure such a danger sign? Can you break that down?
Speaker 1: Sure. Think of it like this. A narrow gap, say less than 25 mm HG difference means the systolic pressure isn't getting very far above the diastolic resting pressure.
Speaker 2: Okay,
Speaker 1: that suggests the heart isn't ejecting much blood with each beat low stroke volume. It's a strong indicator of things like shock or significant fluid loss. The pump isn't generating enough pressure difference.
Speaker 2: That makes sense. Low output.
Speaker 1: Exactly. Now, conversely, a widened pulse pressure, maybe greater than 40 or 50. That can suggest things like aortic regurgitation where blood leaks back creating a big pressure swing or sometimes hyperdamic states like fever or s**** early on.
Speaker 2: Right. Okay, that clarifies it. Now, we can't talk cardiac without talking meds. Let's hit three quick need to know drugs for students.
Speaker 1: Metiprolol, beta blocker.
Speaker 2: Yep. Its job is to lower heart rate and blood pressure.
Speaker 1: So, your main watchouts are bradicardia, slow heart rate and hypotension, low blood pressure.
Speaker 2: Yeah. Especially symptoms like dizziness. Makes sense. Lysinopril, that's an ACC inhibitor, right? The key thing there is potential first dose hypotension. Especially within the first few hours of starting it. Got to monitor that BP closely.
Speaker 1: Okay. And number three, fioamide. Lasix.
Speaker 2: Powerful lipid diuretic. It works fast to pull off fluid, lowering preload, which is great if they're overloaded. But
Speaker 1: yeah, I got to watch that they don't get dehydrated or tank their pressure.
Speaker 2: Exactly. Monitor that HR and BP super closely. They can change fast with IV furosmide.
Speaker 1: Okay. Vitals and meds covered. Now for the part that really requires skill. Oscultation. Listening to the art. Let's start with the basics. S1 and S2, right? S1, that's the lub sound. It's the mitral and tricuspid valves slamming shut at the start of Sisley. You'll hear it loudest down at the apex of the heart.
Speaker 2: Okay, the lub
Speaker 1: and S2, the dub, is the aortic and pulmonic valves closing at the start of diastal. That one's usually clearest up at the base of the heart. And remember, it's normal to hear S2 split slightly into two sounds when the patient takes a deep breath in. That's physiologic splitting,
Speaker 2: right? That's normal. But the ones that really sign trouble. The extra sounds S3 and S4. Let's tackle S3 first. If you hear that, what's the heart telling you?
Speaker 1: S3. It's a low pitch sound. Happens early in diastyl right after S2. Often sounds like Kentucky. You usually need the bell of your stethoscope and often that left lateral position helps.
Speaker 2: Clinically, it usually screams volume overload. The ventricles are resisting rapid filling. It's a classic sign in acute heart failure. Think of it as blood sloshing into a non compliant already full ventricle.
Speaker 1: Okay. Kentucky gallop volume overload. Got it. So, what about S4? That one's late diastal. Right. Just before S1.
Speaker 2: Exactly. S4 is like tendess. It's also low pitched. Heard best with the bell, often at the apex. This sound suggests a stiff ventricle. The atrium is contracting forcefully to push blood into a non-compliant stiff ventricle.
Speaker 1: Stiff like from long-term high blood pressure.
Speaker 2: Precisely. You hear it in conditions like long-standing hypertension, ventricular hypertrophy, or maybe severe aortic stenosis. S3 is often acute volume. S4 is often chronic stiffness or pressure overload.
Speaker 1: That's a helpful distinction. Okay. So to make sure we listen everywhere we need to, we'll quickly run through those oscultation points. The pneummonic APM helps, right?
Speaker 2: It does. So A is for aortic area, second intercostal space, right sternal border. Got it.
Speaker 1: P is pulmonic, second intercostal space, left sternal border. Okay.
Speaker 2: E is herbs point, third intercostal space, left sternal border. Kind of a good spot for hearing both S1 and S2. T is tricuspid fourth interccoal space left sternal border.
Speaker 1: fourth to left.
Speaker 2: and M is mutral or the apical area fifth interpostal space mid-clavvicular line. that's where you find the PMI point of maximal impulse usually.
Speaker 1: perfect. and a quick technique reminder diaphragm first for the higher pitched sounds like S1 S2 then the bell press lightly for low pitched S3 S4 and some murmurss.
Speaker 2: exactly. and move systematically maybe bass to apex or apex to bass but hit all the spots.
Speaker 1: all right let's Talk murmurss. These are sounds of turbulent blood flow. They're graded on intensity scale of I to VI. One is super faint. Six is extremely loud. And while all murmurss need noting for prioritization, the louder ones obviously raise more flags. Where does it become really significant clinically speaking?
Speaker 2: Grade fourth is a key point. That's when the murmur is loud enough that you can actually feel a vibration on the chest wall when you palpate. That's called a thrill.
Speaker 1: Ah, so feeling a thrill means you're dealing with at least a grade the fourth murmur that signifies pretty significant turbulence.
Speaker 2: Definitely. And grade the six, just for context, is so loud you can supposedly hear it with the stethoscope just off the chest. Incredible turbulence.
Speaker 1: Wow. Okay. For students, distinguishing systolic from diastolic murmurss is huge for exams. Systolic ones happen between S1 and S2. Right.
Speaker 2: Correct. And the two classic examples you need to know are micro regurgitation. That's blood leaking back through the mitro valve during cy often radiates towards the armpit, the axilla.
Speaker 1: Okay. MR radiates to the axilla.
Speaker 2: And the other big one is aortic stenosis narrowing of the aortic valve.
Speaker 1: And this is the one with that classic description, isn't it? The one you practically have to memorize for tests.
Speaker 2: That's the one. If you see harsh systolic murmur heard best at the second right intercostal space that radiates to the corateed neck streams aortic stenosis.
Speaker 1: Bingo. That pattern is highly specific. Nail that one down.
Speaker 2: Okay, we'll do. Let's shift from the chest up to the neck. Jugular venus distension. JVD. How do we assess that accurately?
Speaker 1: Right? Remember the positioning. Patient's still at that 30 to 45 degree angle. You're looking for the pulsation of the internal jugular vein. You measure the vertical height from the sternal angle, that bony notch where the manubrium meets the sternum.
Speaker 2: And what's normal?
Speaker 1: Normally, the top of that pulsation should be no more than 3 cm above the sternal angle.
Speaker 2: So, if it's higher than 3 cm, what's that telling us?
Speaker 1: Elevated JVD. More than 3 cm indicates increased pressure in the right atrium, blood is backing up.
Speaker 2: So, think conditions like
Speaker 1: right-sided heart failure is the classic one, but also could be fluid overload for other reasons or even something acute and dangerous like cardiac tamponade where fluid around the heart is squeezing it.
Speaker 2: And connecting this back to treatment, if you see JVD because of fluid overload,
Speaker 1: you're thinking diuretics, right? Especially loop diuretics like fioamide. They help get rid of that excess volume, decrease the preload, and that JVD should come down.
Speaker 2: Okay, let's move out to the periphery. Now, checking circulation all the way out starts with grading those peripheral pulses.
Speaker 1: Yep. Simple but crucial scale. Zero is absent, no pulse. One plus is thready or weak, hard to feel. Yeah. Two plus is considered normal. 3 plus is full or strong. And four plus is bounding really forceful.
Speaker 2: And the absolute key here is checking side to side, right? Bilateral comparison.
Speaker 1: Always compare the radial pulses, the petal pulses, dorsalis pettis, posterior tibial, even popil if needed. Symmetry is key.
Speaker 2: So, what are some quick clinical clues from these grades? Like if you can't find pedal pulses,
Speaker 1: absent pedal pulses, a zero grade, that's a major red flag for peripheral artery disease or P A, blockages in the leg arteries.
Speaker 2: Makes sense. And bounding four plus pulses
Speaker 1: that can suggest states where the heart is pumping really hard or there's a lot of volume moving, maybe fever, sometimes that aortic regurgitation again or even fluid overload. And while you're checking pulses, especially corateed and femoral, listen for brutes, those whooshing. Exactly. Use the bell of your stethoscope. A brute suggests turbulent flow due to narrowing or blockage in that artery. Important finding.
Speaker 2: Okay. Next quick check. Capillary refill. Press the nail bed. See how fast the pink comes back.
Speaker 1: Should be fast. Less than 2 seconds is normal.
Speaker 2: And if it's longer than 2 seconds, delayed refill.
Speaker 1: That points to poor peripheral perfusion. Blood isn't getting out to the fingertips or toes efficiently. You see it in shock, dehydration, severe P A. It's a quick snapshot. of tissue profusion.
Speaker 2: Got it. Last piece in the periphery, edema, swelling. How do we grade pitting edema?
Speaker 1: We press firmly over a bony area like the shin or ankle for a few seconds. The grading is based on how deep the pit is and how long it lasts. 1 plus is a slight pit. Maybe 2 millime disappears quickly. 2 plus is a bit deeper. 4 mm disappears in 10 15 seconds. 3 plus is deeper still. 6 mm might last a minute. And 4 plus is a deep pit. 8 mm or more. And last much longer, like 2 3 minutes or more.
Speaker 2: And does where the edema is give us clues?
Speaker 1: Big time. If it's bilateral, both legs, maybe even sacrum, if they're bedbound, that usually points to a systemic problem. Think heart failure, kidney disease, liver failure, something affecting the whole body's fluid balance.
Speaker 2: Okay. But if it's just one leg, unilateral,
Speaker 1: that makes you think local problem. Top of the list is DBT, a blood clot in the leg vein, or maybe lymphatic obstruction, or even just local inflammation or injury. But unilateral swelling, especially if it's new and painful, needs urgent investigation for DBT.
Speaker 2: Right. And linking edema to meds again for heart failure edema. Besides loop diuretic, sometimes we use moronolactone.
Speaker 1: Yeah, that's a potassium sparing diuretic often used in chronic HF management or if the edema is due to really low protein levels like low albumin in the blood.
Speaker 2: Sometimes they need IVIN to help pull fluid back into the blood vessels.
Speaker 1: Exactly. Treat the underlying cause. Okay, so we've gathered all this physical data. The real skill The thinking like a nurse part is integrating it especially with the electrical picture from the ECG.
Speaker 2: right putting it all together. So if the ECG shows tacic cardia say over 100 BP your next thought is why is it pain fever are they dehydrated hypoalmic got find the cause and if it's bredicardia under 60 first thing check the meds are they on a beta blocker dyoxin calcium channel blocker could be medication induced or is it something else like an heart block okay atrial fibrillation on the monitor regular rhythm, no clear P waves. Priorities shift immediately. First, check the rate. If the ventricular rate is slow, say under 60, you'd likely hold rate controlling meds like dyoxin and critically assess their anti-coagulation status. Aphib carries a high stroke risk.
Speaker 1: Absolutely. And the biggest ECG emergency,
Speaker 2: STEM, ST segment elevation, myioardial inffection. If you see that ST elevation on the ECG,
Speaker 1: that's an acute heart attack. Time is muscle. Kathlab activation MA protocol.
Speaker 2: Yep. Morphine, oxygen, nitro. Glycerin, aspirin, immediate action required.
Speaker 1: This integration piece is really the heart of enclelex prioritization questions, isn't it? Spotting the patterns that signal immediate danger.
Speaker 2: Exactly. Let's run through three critical scenarios.
Speaker 1: Okay. Scenario one. Your patients systolic BP drops below 90 and their heart rate is climbing.
Speaker 2: That combination hypotension plus tacicardia screams shock until proven otherwise. Investigate and intervene fast.
Speaker 1: Scenario two. You oscultate a new S3 heart sound. You see JVD in their neck and you hear crackles in their lungs.
Speaker 2: That triad, acute decompensated heart failure, their fluid overloaded and the heart's failing. Needs urgent diuretics, maybe other support.
Speaker 1: And scenario three, you check peripheral pulses in a leg and they're absent. The leg feels cool to the touch.
Speaker 2: Acute arterial occlusion. A clot has likely blocked blood flow to the limb. That's a vascular emergency. Needs immediate intervention to save the limb.
Speaker 1: Okay. Critical patterns. And quickly, delegation. What can the CNA or tech do versus the RN? CNAs can definitely measure vital signs like BP and report objective findings like patient has swelling in both ankles. They can do routine tasks.
Speaker 2: But the RN
Speaker 1: the RN does the assessment requiring more interpretation. Oscultating heart sounds, interpreting those sounds, interpreting the ECG, judging the significance of JVD, administering IV meds based on these findings. That's RN scope.
Speaker 2: Makes sense. Yeah.
Speaker 1: And finally, patient education. What are the absolute must teach points for cardiac patients going home?
Speaker 2: Daily weights are huge. Teach them to weigh themselves at the same time each day. Same scale, same clothes, and report a gain of more than say 2, three pounds in a day or 5 lbs in a week.
Speaker 1: That signals fluid retention.
Speaker 2: Exactly. Low sodium diet is almost always key, usually less than two grams per day. And strict medication adherence, understanding why they take each med when, and potential side effects like taking carvadil with food to improve absorption.
Speaker 1: Got it. Okay, let's wrap with that sample question. Patient comes in Short of breath, swollen ankles, BP 98/60, heart rate 1 and 12. You find JVD is 5 cm, hear crackles bilaterally, and a new S3 sound. What's the nurse's first move?
Speaker 2: Based on everything we just discussed, notify the provider and get ready to give hurosmite. Right.
Speaker 1: Spot on. This patient is crashing from acute decompensated heart failure. They have low profusion signs, low BP, high HR, and massive fluid overload signs, JBD, crackles, S3. They need that preload reduced urgently with the diuretic delaying that could be fatal.
Speaker 2: Wow. Okay, that really ties it all together. We covered a lot the importance of setup with IPA, those key sounds, S3 and S4, that classic aortic stenosis, murmur description, and really how to synthesize everything to spot acute heart failure.
Speaker 1: Hopefully that gives you a really solid framework, a way to think through it systematically at the bedside.
Speaker 2: Definitely. So, before we sign off, here's something to chew on, a final thought. We know left-sided heart failure often shows up first in the lungs, right? Shortness of breath, crackles,
Speaker 1: and right headed failure often manifests more peripherally JVD edema. So, how might that difference impact the sequence of your assessment in a patient you suspect has heart failure? Which findings give you the most urgent safety information first? Does it change where you start looking or listening?
Speaker 2: H, that's a great question. Something to really maul over in your own practice.
Speaker 1: Absolutely. Well, thank you so much for joining us for this really focused conversation today. Hope it was helpful.
Speaker 2: Yeah. Thanks for listening in. Remember, we'll be back. with more conversations like this each week.
Speaker 1: And don't forget to visit thinklike nurse.org for more great resources and study materials. We'll talk to you next time.