Cardio-Physiology Pt 1: Intro to our body’s Pumping Station

Cardiovascular physiology is primarily focused on getting to know the basic structures of the heart, how these structures work, and what areas are involved in electrical conductivity.

Functions of the Cardiovascular System

Realizing the main functions of the cardiovascular system is necessary for understanding the physiology of the body. With the heart’s intricate pathways of capillaries, arteries, and veins, pumping of oxygen-rich blood, which is one of the primary responsibilities of the cardiovascular system, throughout the body’s entire system is made possible.

Aside from keeping a steady flow of oxygen in the body, the heart and its vessels also perform the following:

  • Transport essential nutrients
  • Remove metabolic toxins and wastes
  • Regulate normal temperature

For more information about how blood flows and distribute oxygen throughout the body, we have prepared a separate video dedicated entirely to that topic. Check it out on our channel.

Hotel Cardiac

Keep in mind that the anatomy portion is different from the electrical part of the heart. So, inside the heart, there are four main chambers, namely:

  • Right atrium
  • Left atrium
  • Right ventricle
  • Left ventricle

We explain every single chamber in a song we’ve created titled, Hotel Cardiac. This is basically a spinoff of the popular song, Hotel California. You can also check the lyrics of that song in our channel so it would be easier for you to memorize and recall how the electrical portion of the cardiovascular system works.

The Rooms

Going back to the Hotel Cardiac song, think of the heart as a four-bedroom suite. Let’s identify each room and what their functions are.

  1. Atriums

As mentioned, the heart has four rooms or chambers, and at the upper portion, there are the attics or what we call as atriums. Atriums are considered as attics because they are comparably smaller than ventricles. These atriums are the receivers of blood either from the rest of the body or the lungs.

  1. Ventricles

Located just below the atriums, the ventricles are the suites of the hearts because they are relatively larger due to their principal objective which is to pump blood to the lungs and out of the heart to the rest of the body. The biggest between the left and right ventricle is the left ventricle which is tasked to pump all the oxygenated blood throughout the various systems. Therefore, if the left ventricle is compromised, the body is doomed.

The Doors

In each of the four bedrooms inside the heart, there are doors which we call valves. These valves are automatic doors that allow blood through the various rooms or suites inside Hotel Cardiac. The sounds, “lub dub,” that are heard when a heart is auscultated are the valves closing.

The Cardiac Gang Sign

The cardiac gang sign, which is just the right hand forming an L like a gun or a loser sign, is a technique that is used to determine the location of the tricuspid and bicuspid valves. By forming an L-shaped figure with your thumb and index finger and closing the rest of the fingers, place the cardiac gang across the chest. Here, you’ll identify that there are two valves at the left side of the heart that is known as the bicuspid valves. On the right side of the heart is where the tricuspid valves are located, which is represented by the three closed fingers.

The Pulmonic and Aortic Valves

The pulmonic and aortic valves create the fundamental sounds that are heard inside the heart. These doors operate through electrical conduction. Currently, the heart is utilizing electricity being transported by the valves.

With that in mind, why is the body not electrocuted? Because the heart is equipped with a zip-lock bag referred to as the pericardium that makes sure electricity flowing inside the heart does not leak to adjacent organs or all over the body.

In part two of our cardiovascular physiology, we will further delve into the process of electrical conduction from one valve and chamber to another. We will tackle the importance of the nodes and branches of the cardiovascular system.

For more nursing-related information that can help you pass major exams, especially the NCLEX®, visit our Simple Nursing website and check out our informative YouTube videos.

Cardiac Output: Stroke Volume, Preload, & Afterload Pt 5

SimpleNursing.com, with Mike Linares, is here once again to turn complicated, frustrating lectures into effortless, piece-of-cake study systems.

Right now, we will be discussing the following:

  1. Cardiac output (CO)
  2. Stroke volume (SV)
  3. Preload
  4. Afterload

Before we go into specifics, let’s first have a quick overview of how the heart functions regarding blood flow regulation.

Heart Regulation of Blood Flow

An average person has about five liters of blood that needs to be circulated throughout the body; therefore, as a pumping organ, if your heart cannot pump the required blood to the rest of the body, what happens? The body gets sick, gets impaired, or eventually dies.

The heart pumps blood throughout the body. Blood carries oxygen and plasma that helps infiltrate the veins and arteries, sustaining blood pressure, thereby sustaining life.

  • Insufficient blood flow = decreased oxygen distribution = tissue death

Think of it as putting a tourniquet around your finger, cutting the blood supply. Immediately, the finger starts to get pale, cold, and cyanotic. Technically, that’s what happens to all parts of the body if blood flow and oxygen are cut off.

Now that you have a better understanding of blood flow regulation by the heart, we go to our main topic.

Cardiac Output

Cardiac output is the amount of blood that’s ejected from the left ventricle, into the aorta of your heart, then out to the rest of the body in one minute.

                        Heart rate x Stroke volume = Cardiac output (one minute)

Stroke Volume

Stroke volume is the amount of blood in one clean pump. How is this seen or applied in the clinical setting?

A client with cardiac failure or congestive heart failure has increased pressure being backed up from the rest of the body because of high blood pressure, so left ventricle struggles to pump out blood to relieve pressure inside the heart. For this reason, stroke volume is decreased because the left ventricle is unable to pump blood efficiently.

Backing up of traffic (too much blood) causes the left ventricle to swell or inflate because it’s trying its hardest to push blood out, going against the resistance of high blood pressure.

  • Decreased stroke volume = compromised cardiac output = left ventricular hypertrophy

How Left Ventricle Hyperinflation is Measured

To determine left ventricular hyperinflation, the lab test of choice is the Brain Natriuretic Peptides (BNP).

When the cardiac output no longer sustains oxygen in the peripheral veins, the brain sends signals to the left ventricle.  Brain natriuretic peptides are compensatory mechanisms of the brain, communicating to the left ventricle, calling out its hyperinflation, and informing it that there is decreased oxygen level inside the body.

There’s a vasomotor center in the brainstem that controls blood pressure, the RAAS system of your kidneys, and the BNP. So BNP is basically telling the left ventricle, “Hey, we need you to take the pressure off.”

  • Normal BNP = less than 100

BNP as high as 300 or more is usually a sign of congestive heart failure (CHF).

Now, when the cardiac output is not meeting the required amount of blood in a minute, and the stroke volume is having a hard time getting pressure off from the heart because of too much resistance, that’s where preload and afterload come in.

Preload

Preload is, in simplest terms, the stretching of ventricles. So ventricles tend to stretch (fill with blood) and squeeze (push out blood). If there is too much pressure filling the ventricles, they tend to extend to the point of not having a proper contraction.

  • Too much stretch = unable to squeeze properly

Afterload

Afterload is the degree of pressure inside the aorta to push or eject blood. Afterload is just a fancy word for the pressure required for the left ventricle to force blood out of the body. So, afterload is just the effort of the ventricle to squeeze. In cases of congestive heart failure (CHF) or hypertension, you have a back-up of pressure on the left ventricle causing it to stretch at great lengths causing a bigger preload and a struggling afterload.

How are increased preload and afterload managed in a hospital setting?

Clients with acute myocardial infarction (MI) are given nitroglycerin and morphine to bring down preload and afterload.

  • Nitroglycerin = relaxes smooth muscle to allow vasodilation
  • Morphine = a central nervous system (CNS) opioid analgesic that relaxes the heart

Hopefully, this was able to help you have a better grasp at one of the trickiest subjects of nursing.

For more useful tips and information, visit SimpleNursing.com. On this site, you can check out our Patho Bible – The Top 70 Diagnoses that are commonly seen in a clinical setting.

Thanks for dropping by!

Peripheral Catheters: Pulmonary Caths explained (SWANS) Pt 5

In this lecture we are going to talk about the following:

  1. Hemodynamics
  2. SWANS catheter
  3. Cardiac output
  4. Pulmonary artery wedge pressure
  5. Atrium pressure (central venous pressure)

Hemodynamics

The main reason for to run a hemodynamics test is to measure four different things:

  1. Vascular capacity – how much pressure is going into the heart
  2. Blood volume – how much volume of blood the heart should push
  3. Pump effectiveness – deals with cardiac output, stroke volume, preload, afterload
  4. Tissue perfusion – concerned with the oxygen that the body consumes

SWANS Catheter

SWANS catheter (pulmonary artery catheter), on the other hand, measures three things, namely:

  1. Pressure
  2. Cardiac output – how much blood the heart pushes in one minute
  3. Oxygen – how much oxygen is going out of the heart

To measure pressure, the doctor inserts the catheter into the right atrium (adjacent to the SA node) and inflates the balloon. Through natural force, the air follows the pressure of the fluid inside the heart and will rest at the pulmonary arteries. Take note that the right side of the heart is responsible for pumping blood directly into the lungs; therefore, the inserted catheter will measure the pressure from the body, into the lungs.

Now, remember, right-sided heart failure is equivalent to body failure. This means that the body does not have sufficient amount of pressure to pump blood into the lungs, causing blood to be forced back into the body, which then leads to edema.

Whereas, if there is a backflow of blood into the left ventricle and goes back into the lungs, there will be the presence of crackles, which is one of the symptoms of left-sided heart failure. Remember that left-sided heart failure can also be considered as a lung-heart failure because the fluid from the heart is being sent back into the lungs.

There are three specific ways to measure the pressure inside the heart.

  1. Right atrial pressure (central venous pressure) – this should be between 1 – 8 mmHg.
  2. PAP (pulmonary artery pressure) – always deflated; resulting in systolic pressure of 15-26 mmHg and a diastolic of 5 – 15 mmHg.
  • Systolic pressure is the squeeze, the force that the heart exerts during contraction (depolarization) and into the lungs and the left ventricle.
  • Diastolic pressure is the decompression or relaxation
  1. PAWP (pulmonary artery wedge pressure) – catheter inflation in the pulmonary artery down to the lungs. Inflation lasts for three to five seconds, cutting off circulation for a quick moment. This will provide a direct measurement of the pressure being back-flowed from the lungs to the prongs. The pressure should be between 4 – 12 mmHg. Furthermore, this measures left ventricular pressure and the diastolic pressure; these are just fancy words for left ventricle “filling time.”

Trivia: in a laboratory setting, this phenomenon is determined by brain natriuretic peptides (BNP). BNP inside the left ventricle helps in the stretching of this specific chamber.

If in case the PAWP is less than 4 mmHg, the client will experience hypovolemia or decreased pressure being pushed into the left ventricle. Hypervolemia, on the other hand, happens if PAWP is more than 12 mmHg; which is also indicative of left ventricular failure.

Example, if your client has 18 mmHg, there will be increased pressure on the left ventricle due to the pooling of blood inside the chamber which causes it to stretch further. The backflow will extend into the right ventricle.

Cardiac Output

Cardiac output (CO) measures the blood flowing into the heart. SWANS measures cardiac output through the thermodilution method which you can remember as the cold choo-choo train.

Take note that normal cardiac output is 4 – 8 L/min. In the thermodilution method, how is that measured with the catheter?

The doctor will pump 5 to 10 ml of cold, normal saline into the catheter, which goes through the heart. The measurement will depend on how fast or how long it took for normal saline to travel into the heart; thus, the cold choo-choo train.

Oxygenation

This measurement basically focuses on how much oxygen is present in the heart and how much oxygen is going back into the lungs. Here, the SVO2 caliber in the catheter is used. Normal SVO2 is between 60% to 80% hemoglobin going back into the lungs. A fiber optic light is used in this type of measurement.

As a recap, a SWANS catheter measures a client’s:

  • Pressure
  • Cardiac Output
  • Oxygenation
  • Heart and blood volume

When is a SWANS catheter (pulmonary artery catheter) used?

SWANS catheter is inserted in clients who underwent cardiac surgery, usually post-CABG. Here, we wanted to observe how the heart is coping with the procedure. Aside from that, SWANS is also inserted in cases of heart failure wherein the doctor has already exhausted all pharmacologic measures like taking volume-depleting drugs which includes ACE inhibitors, Lasix (furosemide), beta-blockers, and calcium-channel blockers.

How is the SWANS catheter inserted?

The client is put on a supine or Trendelenburg position. The doctor will insert the catheter into the jugular vein of the neck or the subclavian vein right under the clavicle or collarbone. From there, the catheter will then be inserted in the right atrium of the heart.

Antihypertensive Medication: Calcium Channel Blockers – Part 2

Calcium channel blockers are antihypertensive medications that technically reduce hypertension or blood pressure; thus, relieving stress from the heart.

How does one quickly spot a calcium channel blocker?

More often than not, calcium channel blockers end in “-pine.” Not to be confused with another antihypertensive medication known as beta-blockers that end in “-lol.” The most popular calcium channel blocker used in a hospital setting, which doesn’t end in “-pine” is Cardizem (Diltiazem). Cardizem drip is given to clients who have significantly high blood pressure and suffers chronic stable angina or chest pain.

Anatomy of the Heart

How do calcium channel blockers relieve the pressure on the heart that results to smooth contraction? All your questions will be answered momentarily but first, let’s do quick anatomy and physiology of the heart.

The heart’s primary responsibility is to pump blood. Think of the heart as a pumping station that pumps fuel to a car, the car is your body. Blood is composed of nutrients as well as oxygen. If the heart is dysfunctional, blood will not be sufficiently pumped, and the organs will malfunction which leads to the deterioration of the system.

Now, the veins vacuum deoxygenated blood into the heart to be re-oxygenated while the arteries send oxygenated blood away from the body. So remember:

  • Veins – Vacuum
  • Arteries – Away

The left ventricle, one of the main chambers of the heart, is the chamber that is mainly responsible for pumping oxygenated blood throughout the entire body. For this reason, the left ventricle is the thickest and the largest chamber of the heart.

If the peripheral vessels (arteries) are stiff, this causes the left ventricle to push hard against the resistance. If this happens, a lot more energy is required, and the left ventricle exerts more stress to pump more blood into the system.

If there was less resistance, the heart does not suffer. The tendency is for the heart to push as much as it can just to suffice different parts of the body with the blood it needs to function correctly. To lessen the strain on the heart and bring the blood pressure down, you need your calcium channel blockers.

How does calcium works inside the body?

Blood vessels are composed of epithelial cells. Imagine that every cell operates as a city – it has walls, a city hall, a cleaning or trash department, a post office, and gates. The central area that we will be focusing on is the city gates which are known as “channels” of the cell. The primary functions of these barriers are:

  • Break down enzymes
  • Allow enzymes into the cell
  • Releases enzymes from the cell

One of the main channels that you want to block in cases of hypertension is calcium. Why do you want to prevent calcium from coming inside the cell? This is because calcium is a mineral that contributes to the following:

  • Cellular connection
  • Blood clot
  • Muscle contraction
  • Nerve function
  • Teeth and bone strength

Calcium hardens the cells which then makes the arteries rigid. Increased cardiac output and stroke volume are two identifiers that the left ventricle is putting a lot of effort to pump blood into the stiff vessels.

Mechanisms of calcium channel blockers

This is where calcium channel blockers come in. Calcium channel blockers prevent calcium from entering the cells which lessens the cell’s hardness thereby making the blood vessels or the highways of the heart more flexible. It is now easier for the left ventricle to push blood out of the heart and into the vessels resulting to lower blood pressure.

For those who haven’t had a copy of the Pathophysiology Bible, get yourself a copy now. It contains more 70 concept maps that you can utilize for your clinical days. Concept maps vary from nursing outcomes, interventions, signs and symptoms, and pathophysiology of the Top 70 diagnoses of common admissions inside the hospital. With the Pathophysiology Bible, your study time will be cut by 200%.

For our next discussion, we will be tackling Nitroglycerin and vasodilators. See you on our next lecture!

 

Antihypertensive Drugs: A Closer Look at Beta-Blockers

Beta-blockers are, in the simplest sense, heart medications for clients with hypertension that is mainly focused on the conduction system of the heart.

Just to refresh your memory, there are two ways to lower blood pressure.

  1. Relieving pressure from the pipes by decreasing fluid volume. These are your ACE inhibitors and diuretics.
  2. Decrease rate of conduction in the heart. These are your beta-blockers and calcium channel blockers.

Mechanism of beta-blockers

Beta-blockers are negative, chronotropic drugs that block that SA node from contracting excessively. Beta-blockers block the beta-adrenergic receptor also known beta-1 and beta-2. Beta-1 are receptors in the heart stimulates increased heart contraction. If stimulated, these beta receptors can cause contraction at higher rates. Similarly, this concept applies to beta-2 in the lungs.

Study tip: Beta-2 is for the lungs (since you have two lungs) and beta-1 is for the heart (since you have one heart)

Beta-2 agonist causes bronchial dilation. One typical example is albuterol. Dosing someone with albuterol will antagonize beta-2. However, it will also affect beta-1 which means that there will be a noticeable rise in your heart rate. This is the reason why treatment of beta-2 causes tachycardia in clients.

Beta-blockers block beta. Beta excited the heart. When the beta is blocked, the heart rate decreases. It’s as simple as that. Cool!

Beta-blockers make you LOL

According to the FDA, identification of these types of drugs must be through their suffix. One of the easiest ways to identify your beta-blockers is to know, by heart, that it can make you laugh out loud (LOL). Meaning, beta-blockers generic names end in –lol. A typical example is atenolol and metoprolol. 

Beta-blocker warnings – the 4 Bs

When giving beta-blockers to your clients, you have to watch out for these adverse effects.

Bradycardia

This is a condition wherein the heart rate of your client drops below 60 per minute. Yes, the goal of beta-blockers is to slow down the heart rate but that doesn’t mean killing your client in the process.

In giving anti-hypertensives, it is advised to give the client the least heavy doses first. Meaning, give your volume depleters first; this will be your diuretics, ACE inhibitors, ARBs, and potassium-sparing diuretics. Don’t opt for electrical or chronological conduction drugs until you have given the volume-depleting drugs and have thoroughly assessed your client’s vitals.

This thought is going to be very useful during exams with borderline, tricky questions. Remember, the most likely answer is holding the drug if the systolic pressure drops to 100.

Blood pressure is decreased

If you’re going to administer a couple of anti-hypertensive drugs, make sure that you ask yourself how safe is it to give. Always run scenarios inside your head especially in terms of the possible out if you gave beta-blockers with other anti-hypertensive drugs. Getting the blood pressure is the best way to assess the necessity of administering the drug. If the blood pressure has significantly dropped after an hour or so, chances are, you won’t be giving the drug.

Yes, we have mentioned that beta-blockers do not decrease blood pressure and only affects Beta-1 in the heart; however, if the stroke volume is decreased, the cardiac output is decreased as well. Low blood pressure is a possible side effect.

Bronchi constriction

Yes, it was mentioned that beta-blockers are for blocking Beta-1; however, there is a probability that Beta-2 can also be blocked. Though it may be specific, it can happen.

Blood sugar masking

If your client has low blood sugar, beta-blockers can mask the signs and symptoms of bradycardia.