Cardiac Anatomy & Physiology Refresher and Heart Failure

Caitlin Hope

Welcome to the show! Today we are going to talk all about the heart — picture a patient who says, "I can't breathe when I lie flat," and before you even touch the MAR, you need the map in your head: four chambers, four valves, and blood moving ONE direction only.

Heather Murphy

That phrase, "one direction only," is the whole thing. Mitral, aortic, tricuspid, pulmonary — four valves acting like one-way doors, so blood doesn't do the equivalent of backing up in hospital hallway traffic.

Derek Mendoza

And if I'm a student trying to visualize it, I always wanna slow it down. Start me at the vena cava, which is located on the upper right side of the heart. Deoxygenated blood flows through the superior (upper) and inferior (lower) vena cava and into the right atrium (that's the upper right chamber of the heart). The right side of the heart is the receiver of blood. So now where does that dark, deoxygenated blood go next?

Heather Murphy

Superior and inferior vena cava into the right atrium, through the tricuspid valve to the right ventricle (that's the right lower chamber of that heart). Once the deoxygenated blood flows through the right ventricle, it travels up and out to the lungs via the pulmonary valve. What do you think happens to the blood once it hits the lungs? RIGHT! It gathers oxygen and becomes oxygenated blood. That oxygenated blood comes back to the heart by the pulmonary veins into the left atrium. The blood then crosses the mitral valve into the left ventricle (that left lower chamber). From there the oxygenated blood flows out the aortic valve to the body through the aorta. As the ventricles squeeze, blood shoots out of it like a rocket. It's like a giant roller coaster ride of blood. If you learn that sequence, it makes understanding the heart much easier. THINK: right heart to the lungs, left heart to the body. If you lose that sequence, heart failure gets really hard to understand.

Caitlin Hope

So the pulmonary veins bring oxygenated blood directly into the LEFT atrium. And now we understand those S1 and S2 sounds we learned in assessment class. S1 is that "lub" which is the atrial valves closing. S2 is that "dub" which is the ventricle valves closing.

Heather Murphy

Yes, and one more layer: the coronary arteries are the first two branches off the aorta, so the myocardium gets its own blood supply right away. That's clinically important because if the muscle is injured, the pump suffers.

Caitlin Hope

Exactly. And now to talk about the electrical part of the heart. Something has to make those chambers squeeze to send that blood through the roller coaster ride. That is the conduction system of the heart. The conduction system is specialized cells carrying the impulse: SA node (sinoatrial node) in the right atrium sends a signal to the AV node, then to the bundle of His, down the right and left bundle branches, and out through Purkinje fibers. Electrical DEPOLARIZATION triggers contraction and ejection of blood from the ventricles. When the myocardium relaxes, the ventricles have time to fill back up.

Derek Mendoza

Wait — SA node, AV node, bundle branches, Purkinje. So the ECG is basically the tracing of that electrical story, but the actual blood movement is the mechanical result?

Heather Murphy

Yes — that's a clean way to say it. ECG answers, "How is the electrical system behaving?" It can show rhythm abnormalities or conduction problems. But it does NOT directly tell you ejection fraction or valve structure. Students sometimes over-assign meaning to the ECG.

Caitlin Hope

Professor Murphy, grab that distinction with the other tests, because this shows up on exams and at bedside handoff all the time.

Heather Murphy

Sure. Troponin or CK-MB labs answers, "Is there myocardial injury?" B-type natriuretic peptide, known as BNP is a hormone produced by the heart and a high amount can mean heart failure. BNP answers, "Could this dyspnea be cardiac rather than respiratory?" Echocardiogram answers, "What does the heart look like and how well is it pumping and filling?" — chamber size, valves, septal motion, pericardial sac, and ejection fraction. ECG answers, "What's the rhythm and conduction doing?" Four different questions. Do not flatten them into one bucket called "cardiac labs and tests."

Derek Mendoza

I like that — four tests, four questions. Because if a patient is short of breath, BNP helps you sort cardiac versus respiratory cause of dyspnea. That's a very different question from troponin asking about injury.

Caitlin Hope

Yep. And now mechanics. Systole is contraction — ventricles eject blood. Diastole is relaxation — ventricles fill. Stroke volume is blood ejected with each beat. Cardiac output is stroke volume times heart rate: CO equals SV times HR. If either piece drops enough, tissue perfusion drops.

Derek Mendoza

CO equals SV times HR — that formula is like the recipe card. But the ingredients that change stroke volume... that's preload, contractility, and afterload, right?

Caitlin Hope

Right. Preload is the volume in the ventricles at the END of diastole — how much stretch before the squeeze. Afterload is the resistance the left ventricle has to pump against. Contractility is the muscle's squeeze strength. In heart failure, those three stop being abstract words real fast. A quick memory trick: **preload = before the load** — think volume filling the ventricle before it contracts; **afterload = after the load** — think the resistance the ventricle has to push against when it ejects. Another easy version is **preload = stretch, afterload = push**. So preload is about filling, and afterload is about resistance to outflow.

Heather Murphy

And bedside numbers matter because they hint at those forces. Normal blood pressure is less than 120 over less than 80. Mean arterial pressure — MAP — needs to stay over 60 millimeters of mercury to sustain vital organs in the average person under most conditions. MAP is the number that makes you ask, "Are the kidneys and brain getting enough pressure?"

Derek Mendoza

Over 60 for MAP — so if I see a pressure that doesn't look terrible at first glance, I still need to think, "Is organ perfusion actually protected?" That's the hidden question.

Caitlin Hope

Yes, and nurses miss that when they stare only at systolic. I've had new grads tell me, "The BP is okay-ish," and then the patient has cool skin, low urine output, and is heading toward a bad night. Numbers are clues, not the whole patient.

Heather Murphy

Also remember the autonomic piece. Sympathetic stimulation increases heart rate, AV node conduction speed, and force of contraction. Parasympathetic stimulation decreases heart rate. Early on, that sympathetic push can look helpful. Later, in heart failure, it becomes part of the problem.

Derek Mendoza

And that's the tension in heart failure, isn't it? The body is trying to save itself. RAAS (a critical hormone system that increases blood pressure and blood volume when renal perfusion is low) and the sympathetic nervous system switch on to maintain cardiac output... until that rescue becomes harmful.

Heather Murphy

Exactly. At first, compensation can maintain enough cardiac output for tissue perfusion — that's compensated heart failure. But chronic RAAS and SNS stimulation leads to sodium and water retention, inflammatory activity, ventricular remodeling, and even interruptions in electrical conduction. The same systems that prop up perfusion for a while can eventually worsen congestion and pump failure.

Caitlin Hope

And that sodium-water retention is the part students can SEE. More fluid means more volume backing up. Most commonly it's left-sided heart failure from left ventricular dysfunction, so blood backs up into the left atrium and pulmonary veins. That is why you get pulmonary congestion and edema. Think LEFT= LUNGS.

Derek Mendoza

Pulmonary veins backing up into the lungs — that's why the patient says, "I can breathe sitting up but not flat." Orthopnea isn't just a vocabulary word. It's a plumbing problem.

Heather Murphy

Well said. And here's the classification piece: HFrEF is heart failure with REDUCED ejection fraction — the heart can't pump effectively. HFpEF is heart failure with PRESERVED ejection fraction — the ventricles have impaired relaxation and filling during diastole. Different mechanics, but BOTH can lead to impaired cardiac output.

Caitlin Hope

Let me say it back in bedside language. HFrEF: weak squeeze. HFpEF: stiff fill. One way to remember is to try this: **HFrEF = Heart Fails to Eject** — the squeeze is weak, so the ejection fraction is reduced. **HFpEF = Heart Fills but can’t relax** — the ventricle is stiff, so the ejection fraction is preserved even though filling is the problem. A quick shortcut is **R = Reduced squeeze** and **P = Preserved but stiff**. So if you hear HFrEF, think weak pump; if you hear HFpEF, think stiff ventricle. Not perfect, but for exam thinking, that gets you close.

Heather Murphy

Close, yes. And useful. Just remember both can leave the patient fatigued, short of breath, and exercise intolerant. And this is where the left-sided versus right-sided distinction really helps. Left-sided heart failure is mostly a left ventricle problem, so blood backs up into the left atrium and then into the pulmonary veins. That means lung symptoms: dyspnea, orthopnea, crackles, pulmonary edema, and sometimes frothy, pink-tinged sputum when things are severe. If the left side cannot move blood forward, the lungs become the backup zone. Right-sided heart failure is mostly a right ventricle problem, so blood backs up into the systemic venous circulation. That gives you systemic congestion: jugular venous distension, hepatomegaly, ascites, dependent edema, weight gain, and sometimes a feeling of abdominal fullness or right upper quadrant discomfort. Think body swelling, not just breathing problems. Here’s a memory trick: LEFT = LUNGS, RIGHT = REST OF the body — or even "left leaks to the lungs, right swells the body." A lot of patients have both, but if you’re trying to sort the first big clue, ask yourself: are the symptoms mostly in the lungs, or mostly in the legs and belly? Left-sided failure backs up into the lungs. Right-sided failure backs up into the body.

Derek Mendoza

What tends to show up first when chronic heart failure decompensates?

Heather Murphy

Signs of fluid retention — weight gain, exertional dyspnea, orthopnea. Patients newly diagnosed with HF are more likely to present with pulmonary edema. Chronic findings can include fatigue, cough, dyspnea, tachycardia, edema, and limits in usual ADLs.

Caitlin Hope

And at bedside, the "don't-miss" cluster is crackles, jugular venous distension, edema, increasing dyspnea, and weight gain. If a patient tells me their shoes got tight, they needed three pillows last night, and they're up a few pounds... I am not waiting for that to magically improve.

Derek Mendoza

Three pillows. That's such a concrete image. And the teaching number from the guideline here is call the provider for a weight gain of 3 pounds over 2 days or 3 to 5 pounds over a week. That's memorable because it's so specific.

Heather Murphy

Yes — daily weights are not busywork. They are trend data. Same scale, same time, similar clothing if possible. That can catch decompensation before the patient is in full distress.

Caitlin Hope

Professor Murphy, can you hit warm and cold, wet and dry? Because once students see that grid, acute decompensated heart failure gets a lot less fuzzy.

Heather Murphy

Sure. "Wet" means congestion is present. "Dry" means no congestion. "Warm" means perfusion is adequate. "Cold" means low perfusion. So wet-warm: congested, but cardiac output is still okay — often dyspnea, edema, orthopnea. Dry-warm: no congestion, perfusion okay. Dry-cold: low output without major congestion — think edema can still appear, hypotension, cool extremities. Wet-cold is the dangerous combination: congestion plus low output, with altered mental status, decreased oxygen saturation, reduced urine output, even shock.

Derek Mendoza

Wet-cold. That phrase alone feels like an alarm bell — fluid overloaded AND poorly perfused.

Caitlin Hope

It is. That's your NCLEX-style pause and prioritize moment. Assess oxygenation, breath sounds, mental status, urine output, pulse ox, blood pressure, and how hard the patient is working to breathe. Then think intervention based on the problem in front of you.

Heather Murphy

For acute decompensated HF, goals include symptom relief, optimizing volume status, supporting oxygenation and ventilation, supporting cardiac output and end-organ perfusion, identifying the cause, avoiding complications, teaching, and discharge planning. Treatment strategies include diuretics or ultrafiltration to decrease intravascular volume, reducing preload, reducing afterload with vasodilators to improve cardiac output and decrease pulmonary congestion, and supplemental oxygen. Inotropes and hemodynamic monitoring may be needed if the patient does not respond or is in cardiogenic shock.

Derek Mendoza

And anxiety matters here too, right? Because if the sympathetic nervous system is already flooring the gas pedal...

Caitlin Hope

...then panic makes it worse. Yep. Reducing anxiety is nursing care, not a soft extra. Less SNS surge means less myocardial workload. I've seen a patient breathe easier just from upright positioning, oxygen as indicated, clear coaching, and getting the right meds moving.

Heather Murphy

For chronic heart failure, especially HFrEF, therapy focuses on symptom management, reducing mortality and morbidity, improving quality of life, and monitoring response to evidence-based therapies. ACE inhibitors are primary drugs for chronic HFrEF. ARBs may be used if ACE inhibitors are not tolerated. Beta-blockers with ACE inhibitors improve survival and reverse ventricular remodeling. Aldosterone antagonists reduce mortality and hospitalization. Diuretics reduce edema, pulmonary venous pressure, and preload.

Derek Mendoza

And on the teaching side, patients need to know how to take a pulse, when drugs like digitalis and beta-blockers may need to be held and the provider called, how to monitor BP at home, and how to recognize fluid overload early.

Caitlin Hope

Plus sodium teaching. Edema is often treated by restricting dietary sodium. Fluid restriction isn't usually prescribed for mild to moderate HF, but it may be used in severe HF and renal insufficiency. So don't overteach a blanket fluid rule that isn't actually ordered.

Heather Murphy

And for end-stage HF, this is where advanced options enter: mechanical circulatory assist devices such as ventricular assist devices, palliative care, hospice, and for selected patients, heart transplantation. VADs can support the left, right, or both ventricles and may bridge recovery, surgery, or transplant. The goal of care for HF patients is to decrease symptoms, decrease peripheral edema, increase exercise tolerance, adhere to treatments, and reduced complications.

Derek Mendoza

So the useful takeaway for a student is this: when you see heart failure, ask two questions fast — where is the blood backing up, and is the patient still perfusing? If you can answer those two, your assessment and your next nursing move get a whole lot clearer.

Heather Murphy

I know this was a lot of information in a short amount of time, but do not get discouraged. Listen to this podcast again and follow along with the packet, key points, PowerPoints, and other reference materials you find. Repetition helps retention! Until next time, take care of your own heart!