Hemodynamics

Let’s start with the central equation of life. How much blood is actually moving through the body?

Cardiac output equals heart rate multiplied by stroke volume.

It is wonderfully simple. Cardiac output is the volume of blood pumped by the heart in one minute. In a normal, healthy state, normal cardiac output ranges from 4 to 8 liters per minute in a resting adult. To get that number, the heart relies on two things: how fast it beats (Heart Rate) and how much it pushes with each beat (Stroke volume is the amount of blood ejected by the left ventricle during each contraction).

Source: 2036 Summary of Factors in Cardiac Output by OpenStax College, CC BY 3.0.

But what determines stroke volume? Three brilliant mechanical concepts: Preload, Afterload, and Contractility.

1. Preload (The Stretch)

Imagine stretching a rubber band. The further you stretch it, the harder it snaps back. That is exactly what happens in the heart. Preload is the degree of myocardial fiber stretch at the end of ventricular diastole (right before it squeezes).

Nature has a neat trick up her sleeve here: increased preload increases stroke volume up to a physiological limit. If you stretch the heart with more venous return, it contracts harder. But stretch it too much, and the rubber band loses its elasticity—that's heart failure.

2. Afterload (The Resistance)

Now imagine trying to blow water out of a tiny straw versus a wide garden hose. The resistance you feel? That’s afterload. Afterload is the resistance the ventricles must overcome to eject blood.

3. Contractility (The Muscle)

Even with perfect preload and afterload, the muscle itself has to be strong. Contractility is the inherent strength of the myocardial contraction.

Pharmacological Fine-Tuning

When the physics gets out of balance, we use drugs to manipulate the pump and the pipes:

• Vasodilator medications decrease systemic vascular resistance, opening the pipes to make pumping easier.
• Vasopressor medications increase systemic vascular resistance, clamping down the pipes to keep blood pressure up.
• Positive inotropic medications increase myocardial contractility, making the heart muscle squeeze with more vigor.
• Negative inotropic medications decrease myocardial contractility, allowing the heart to rest and require less oxygen.

How do we measure all these forces inside a living patient? We drop sensors into the pipes.

To measure the right side of the heart, we look at the venous return. Central venous pressure measures right ventricular preload. What’s a healthy stretch for the right side? Normal central venous pressure ranges from 2 to 8 millimeters of mercury.

To measure the resistance the left ventricle fights, we use the arteries. Systemic vascular resistance measures left ventricular afterload. Conversely, the right ventricle has to push into the lungs, so pulmonary vascular resistance measures right ventricular afterload.

When we need to know exactly what is happening deep inside the heart, we thread in a special line. A pulmonary artery catheter measures right-sided heart pressures. But the real trick is the balloon at the end. When we inflate it, pulmonary artery wedge pressure provides an indirect measurement of left atrial pressure.

Source: Pulmonary artery catheter english by derivative work: Tariq Abdulla ( talk ) Pulmonary_artery_catheter_german.jpg : User:Chikumaya , modifizert von PhilippN Pulmonary_arterial_catheter.svg : User:Chikumaya, CC BY-SA 3.0.

Normal pulmonary artery wedge pressure ranges from 6 to 12 millimeters of mercury.

If that number is high, fluid is backing up. An elevated pulmonary artery wedge pressure indicates left ventricular failure, or, more simply, an elevated pulmonary artery wedge pressure can indicate fluid volume overload.

The Phlebostatic Axis: The Crucial Zero Point

All these pressure readings are useless if the sensor isn’t perfectly leveled to the heart. We level our equipment to the phlebostatic axis, which is located where the fourth intercostal space meets the midaxillary line.

This is basic physics: hemodynamic pressure transducers must be leveled to the phlebostatic axis for accurate readings.

• Leveling a hemodynamic transducer above the phlebostatic axis produces falsely low pressure readings (gravity pulls the fluid down away from the sensor).
• Leveling a hemodynamic transducer below the phlebostatic axis produces falsely high pressure readings (gravity pushes extra fluid weight onto the sensor).

When cardiac output drops, the body panics and tries to save the brain and the heart.

First, we look at overall systemic pressure. Mean arterial pressure is the average pressure in the systemic circulation throughout the cardiac cycle.

Mean arterial pressure equals the sum of the systolic pressure plus twice the diastolic pressure divided by three.

To keep the organs alive, a mean arterial pressure of at least 65 millimeters of mercury is required for adequate organ perfusion.

If cardiac output begins to fail, the body triggers a cascade of alarms:

1. Tachycardia is a compensatory mechanism to maintain cardiac output. (If the stroke volume is low, the heart beats faster to make up for it!)
2. A decreased level of consciousness is an early clinical sign of decreased cardiac output. (The brain is exquisitely sensitive to a lack of oxygen).
3. Cool extremities indicate peripheral vasoconstriction secondary to decreased cardiac output. (The body shunts blood away from the fingers and toes to save the core).
4. Oliguria indicates poor renal perfusion associated with decreased cardiac output. (The kidneys stop making urine because they aren't receiving enough blood flow).
5. Hypotension is a late clinical sign of decreased cardiac output. (By the time the blood pressure drops, the compensatory mechanisms have completely failed).

If this downward spiral isn't stopped, the patient enters cardiogenic shock, which is a severe state of decreased cardiac output despite adequate intravascular volume. The tank is full, but the pump is fundamentally broken.

How broken? We check the "squeeze" percentage. Normal left ventricular ejection fraction ranges from 55 to 70 percent. However, an ejection fraction less than 40 percent indicates significant left ventricular dysfunction.

When the ventricles are failing and stretching out of shape, they secrete a distress hormone. B-type natriuretic peptide levels elevate in response to ventricular stretching. So, if you run lab work, a B-type natriuretic peptide level greater than 100 picograms per milliliter indicates heart failure.

Source: Right side heart failure by http://www.scientificanimations.com, CC BY-SA 4.0.

The heart’s mechanical pump is useless without its electrical pacemaker. To monitor this, we use telemetry. Telemetry monitoring requires intact skin free of excess hair for optimal lead adherence.

You must place the leads perfectly to get a clear picture. Memorize this classic placement pattern:

• The white telemetry lead is placed on the right upper chest. (White on Right)
• The black telemetry lead is placed on the left upper chest. (Smoke over Fire)
• The red telemetry lead is placed on the left lower chest. (Fire)
• The green telemetry lead is placed on the right lower chest. (Snow over Grass)
• The brown telemetry lead is placed near the center of the chest. (Chocolate in the middle)

The Normal Rhythms

A beautiful, normal rhythm has strict timing:

• A normal PR interval ranges from 0.12 to 0.20 seconds.
• A normal QRS complex duration ranges from 0.04 to 0.10 seconds.
• A normal QT interval is typically less than 0.40 seconds.

The baseline itself tells a story about oxygen. ST-segment depression on an electrocardiogram indicates myocardial ischemia (the heart is starving for oxygen). Worse yet, ST-segment elevation on an electrocardiogram indicates acute myocardial injury (the tissue is actively dying).

The Electrical Glitches

When the wiring goes haywire, you must recognize it instantly.

The Sinus Rhythms:

• Sinus bradycardia is defined as a regular rhythm with a heart rate less than 60 beats per minute. If the patient is dizzy and passing out, Atropine is the primary medication for treating symptomatic bradycardia.
• Sinus tachycardia is defined as a regular rhythm with a heart rate greater than 100 beats per minute.

The Atrial Chaos:

• Atrial fibrillation exhibits an absence of distinct P waves on an electrocardiogram and presents with an irregularly irregular ventricular rhythm. Because the atria are quivering, blood pools. Therefore, atrial fibrillation increases the risk of systemic thromboembolism (strokes).

Source: Atrial Fibrillation by BruceBlaus, CC BY-SA 4.0.

• Atrial flutter presents with characteristic sawtooth waves on an electrocardiogram.
• If the upper heart is racing stably (SVT), Adenosine is the first-line medication for stable supraventricular tachycardia. Because it metabolizes in seconds, Adenosine must be administered as a rapid intravenous push.

The AV Blocks (The Delays):

• First-degree atrioventricular block exhibits a constant PR interval greater than 0.20 seconds. (Just a steady delay).
• Second-degree atrioventricular block type I exhibits a progressively lengthening PR interval until it eventually drops a QRS complex. (Long, longer, drop—that is a Wenckebach).
• Second-degree atrioventricular block type II exhibits a constant PR interval with intermittently dropped QRS complexes. (Highly unpredictable and dangerous).
• Third-degree atrioventricular block is characterized by a complete lack of electrical conduction from the atria to the ventricles. The atria and ventricles are beating entirely independently. This is an emergency! Third-degree atrioventricular block requires immediate pacing.

The Ventricular Nightmares (Life Threats):

• Premature ventricular contractions are early beats with wide QRS complexes. A few are okay, but frequent premature ventricular contractions can lead to ventricular tachycardia.
• Ventricular tachycardia presents with wide QRS complexes at a rate greater than 100 beats per minute. If they lose their pulse, pulseless ventricular tachycardia requires immediate defibrillation.

Source: Electrocardiogram of Ventricular Tachycardia by The original uploader was Ksheka at English Wikipedia ., CC BY-SA 2.5.

• Ventricular fibrillation exhibits a chaotic baseline without identifiable QRS complexes. The heart is just quivering; there is zero cardiac output. Ventricular fibrillation requires immediate cardiopulmonary resuscitation and requires immediate defibrillation.

• Asystole presents as a flat line on an electrocardiogram indicating an absence of electrical activity. Do not shock a flatline! Defibrillation is not a valid treatment for asystole. Instead, Epinephrine is the primary pharmacological treatment for asystole.

When medications fail, we use electricity and hardware.

Electricity: Defibrillation vs. Cardioversion

You must understand the difference between these two life-saving shocks.

• Defibrillation delivers an unsynchronized electrical shock to the myocardium. It blasts all the cells at once, hoping the primary pacemaker resets.
• Synchronized cardioversion delivers a shock synchronized with the R wave on the electrocardiogram. We do this for rhythms like unstable SVT or Atrial Fibrillation. Why synchronized? Because delivering a shock on the T wave can precipitate ventricular fibrillation. Crucially, synchronized cardioversion requires the client to have a palpable pulse.

Hardware: Pacemakers and Devices

When the heart's natural pacemaker is broken, we install our own. A pacemaker delivers electrical impulses to stimulate myocardial contraction.

On the EKG, you will see a sharp vertical line called a pacing spike.

• A pacing spike immediately preceding a P wave indicates atrial pacing.
• A pacing spike immediately preceding a QRS complex indicates ventricular pacing.

There are several ways to pace a heart:

1. Transcutaneous pacing involves delivering electrical impulses through pads placed on the chest wall. This is painful, so transcutaneous pacing is a temporary intervention for symptomatic bradycardia.
2. Transvenous pacing involves threading a pacing wire through a central vein into the right ventricle.
3. Epicardial pacing wires are placed directly onto the heart muscle during cardiac surgery.

When using a transcutaneous pacemaker, how do you know it's working? The energy setting for transcutaneous pacemakers is increased until mechanical capture is achieved. You look at the monitor: Electrical capture on an electrocardiogram is evidenced by a pacing spike followed by a QRS complex. But EKG capture isn't enough; you need an actual pulse! Assessing the femoral pulse is the preferred method to verify mechanical capture during transcutaneous pacing.

Source: True-capture by Rblumel, CC BY-SA 4.0.

Sometimes, pacemakers malfunction.

• Pacemaker failure to capture occurs when a pacing spike is not followed by a myocardial contraction. (The wire fired, but the heart ignored it).
• Pacemaker failure to sense occurs when the device fires electrical impulses at inappropriate times. (It is ignoring the heart's native rhythm).

Patient Safety Note: Clients with a newly implanted pacemaker must restrict arm movement on the operative side to prevent dislodging the fresh wires. Also, magnetic resonance imaging is generally contraindicated for clients with traditional pacing devices.

For patients with lethal arrhythmias, we implant a bigger safety net. An implantable cardioverter-defibrillator detects life-threatening ventricular arrhythmias and automatically delivers a shock to restore normal sinus rhythm.

Source: Blausen 0543 ImplantableCardioverterDefibrillator by Jmarchn, CC BY-SA 3.0.

The Ultimate Plumber's Tool: The IABP

If the heart is failing fundamentally (like in cardiogenic shock), we use a balloon to help pump the blood. The intra-aortic balloon pump is a mechanical circulatory support device. It sits in the aorta and works in total synchronization with the heart:

• An intra-aortic balloon pump inflates during diastole to increase coronary artery perfusion. (Pushing blood backwards into the heart muscle).
• An intra-aortic balloon pump deflates right before systole to decrease afterload. (Creating a vacuum effect that makes it incredibly easy for the weak left ventricle to eject blood).

If hemodynamics fail, the kidneys fail. When this happens, we have to artificially replace renal function.

Hemodialysis relies on diffusion to remove waste products from the blood, and it relies on ultrafiltration to remove excess fluid from the blood.

Source: Hemodialysis-en by G YassineMrabet Talk ✉, CC BY-SA 3.0.

The AV Fistula

To move massive amounts of blood, we surgically sew an artery and a vein together. An arteriovenous fistula requires weeks to mature before hemodialysis use.

You must protect this lifeline. To check if it is working:

• A palpable thrill over an arteriovenous fistula indicates functional patency. (It feels like a purring cat under the skin).
• An audible bruit over an arteriovenous fistula indicates functional patency. (It sounds like a whooshing river through your stethoscope).

To protect it: Blood pressure measurements must not be taken on an arm with an arteriovenous fistula, and venipuncture must not be performed on an arm with an arteriovenous fistula.

Dialysis Complications

Removing 3 liters of fluid in 4 hours takes a toll. Hypotension is the most common complication during hemodialysis treatments.

If we remove waste products too quickly, the brain's osmolarity gets entirely out of balance, pulling fluid into the skull. Dialysis disequilibrium syndrome can present with severe headaches and can manifest as neurological confusion.

Continuous Renal Replacement Therapy (CRRT)

What if a patient is in cardiogenic shock and their mean arterial pressure is 60? Standard dialysis will bottom out their pressure and kill them.

Enter CRRT. Continuous renal replacement therapy is indicated for hemodynamically unstable clients because continuous renal replacement therapy provides slow fluid removal to minimize hemodynamic compromise.

Instead of doing it in 4 hours, it runs 24/7. Continuous venovenous hemofiltration removes large volumes of fluid continuously over 24 hours.

Because blood is sitting in a machine all day, it wants to clot. Regional anticoagulation with citrate is often used to prevent filter clotting during continuous renal replacement therapy. But there's a catch: citrate binds to calcium to stop the clotting cascade. Therefore, calcium levels must be closely monitored during continuous renal replacement therapy using citrate anticoagulation to ensure the patient doesn't develop severe hypocalcemia.

Final Thoughts for the Exam

When you sit down for the NCLEX, remember that hemodynamics is logical. Tracing the path of the blood, calculating the stretch and resistance, watching the electrical delays on the EKG, and protecting the fragile balance of fluid shifts—it all follows the beautiful, predictable laws of physics. Understand the pump, protect the pipes, and you will do exceptionally well.