HIV/AIDS

 **Most of this information is complied by that given in the ATI Med-Surg book (pages 1006-1015) and the HIV/AIDS ppt lecture uploaded in CourseDen

Opening Note

I've decided to create this blog as a tool for me (and maybe a few other nursing students) to use as a resource out here in cyberspace. I'm going to attempt to review all the information we've learned in the Adult Health class and cover all the topics therein. 

Why am I doing this? Because it's very easy to forget bits and pieces, especially with the load of information we receive in lecture.

I'm going to start with Cardiac because, personally, I feel it's my weakest area. My hope is that reviewing all the information and writing it down will reinforce the ideas and concepts.

This blog has being created by a Nursing student at University of West Georgia, class 2011.

What's that Sound?

What can you expect to hear in patients with valve disorders?

First, a short description of each valvular disorder:

• Aortic Stenosis: the aortic valve orifice narrows and obstructs the left ventricular outflow during systole. Increased resistance to ejection or afterload result in ventricular hypertrophy.

• Aortic Regurgitation: the aortic valve leaflets do not close properly during systole leading to leakage (or regurgitation) back into to left ventricle.

• Mitral Stenosis: valve leaflets fuse and stiffen while the chordae tindineae (the white string looking parts in the picture below) contract and shorten.

• Mitral Regurgitation: the mitral valve is prevented from closing completely during systole, allowing back-flow into the left atrium.

• Mitral Valve Prolapse: leaflets enlarge and prolapse (slip out of place) into the left atrium during systole. Usually benign, but in some cases may progress to mitral regurgitation.

Need a visual?

Notice that the valves in the image above are rather close together. This might lead you to believe they would be hard to distinguish from each other - however, auscultation of the aortic valve and mitral valve are in two VERY different places.

As you can see in the picture above, the Mitral area or apex of the heart is found on the left at the 5th intercostal space along the midclavicular line. If you've a patient with larger breasts, you may have to put on gloves and move it to the side to hear properly.

The Aortic area is to the right of the chest at the 2nd intercostal space near the sternum. Notice that the area nearly lines up vertically with the bony prominences on the clavicle. 

Always pay attention to landmarks when auscultating!

The next thing to ask is what do these valvular disorders sound like?

 Let's listen to a normal heart sound for the sake of better comparison. This link will open a youtube video for easier listening. Make sure to read the notes on the video.

Normal Heart Sounds 

Note that the sounds in the video mimic what can be heard at the mitral area.

Easy enough, right?

Moving on, here's what a case of mild aortic regurgitation can sound like. Once again, make sure to read the notes on the video - they can be really helpful in explaining what and why it sounds like that.

Mild Aortic Regurgitation

 Remember: Regurgitation is the back-flow of blood! Blood is a fluid! So listen for the sound of flowing fluid - One cardiologist described it to me as "water swishing in a washing machine".

And where do you go to hear this?

Second right intercoastal space next to the sternum!

This is Aortic Stenosis. It can be heard in a diamond shape at the aortic area and comes across as a harsh crescendo-decrescendo during systole. Different source, so there's no notes to read with this one; but do pay attention to what the narrator says in the video as it can be very helpful.

Aortic Stenosis

Notice that the murmur is at the end of the lub part of lub dub.

Mitral Stenosis is a rumbling, apical diastolic murmur. Apical meaning, of course, at the apex of the heart, also known as the mitral area at the 5th intercoastal space! The video quality on this one is a little rougher than previous. Listen closely - there are three different examples. They will sound very similar to the Aortic Stenosis, but the murmur is on the dub of lub dub.

Mitral Stenosis

Mitral Regurgitation is a high-pitched systolic murmur at the apex of the heart that can sometimes radiate to the left axilla. Severe regurge results in S3. Once again, the video quality is a little rough. The Mitral Regurgitation sounds very similar to Aortic Regurgitation at first.

Mitral Regurgitation

Notice that the murmur is on the lub part of lub dub. Remember that regurgitation is back-flow of blood and will sound similar to water swishing!

Last but not least, we have the Mitral Valve Prolapse. What you should hear is a midsystolic click - it's very obvious in the video. Mitral prolapse may also have a late systolic murmur that can be heard at the apex of the heart.

Mitral Valve Prolapse

How do you remember whether the murmur can be heard in diastole or systole?

Well, luckily acronyms are to the rescue once again. This is how I remember:

Diastole  =  "Dammit, Always Read Maps Straight"

(Aortic Regurgitation, Mitral Stenosis)

Systole  =  "Secret: Artie Says Men Read More Porn"

(Aortic Stenosis, Mitral Regurgitation, Mitral Prolapse)

Are they the most clever or elegant of devices? No, not at all. 

Should you say either of these out loud during a test? I wouldn't recommend it. 

But, if they help you remember then they've done their jobs. Don't like these? Think up your own! It's always easier to remember something if you have to think of it yourself. Only you truly understand your brain and what will help you remember.

Heart Failure [Part III]

HOW THESE DISEASES LEAD TO HEART FAILURE

 

FYI: Could this be the future of treating hypertension? Maybe for some: LOWERING BLOOD PRESSURE DRUG FREE

Heart Failure [Part II]

HOW THESE DISEASES LEAD TO HEART FAILURE:

Now let's look at Myocardial Infarction (aka Heart Attack)

[Edit] While still in the experimental phase, the lost tissues may be able to be regenerated with certain stem-cell secreted protein: CLICK HERE

Heart Failure [Part I]

HEART FAILURE is the inability of the heart to maintain proper circulation, leading to tissue perfusion inadequacies.

What can cause it:
Multiple things! However, I will be focusing on:

Coronary Artery Disease (CAD)

Myocardial Infarction (MI)

Hypertension (HTN)

&

Valvular Disease



Let's start with Coronary Artery Disease.

FYI: Did you know that CPR technique suffers during the night? CLICK HERE FOR MORE INFORMATION

Cardiac Output

If you only learn one thing from the cardiac content, make sure it's this:

Cardiac Output = Heart Rate x Stroke Volume

It's kind of a big deal.

But what does it mean, really? 

Well, cardiac output as defined by the Iggy textbook is the measurement of blood flow from the heart into the systemic arterial circulation. You can also think of it as the amount of blood pumped from the left ventricle each minute. 

It helps to think of it like this: Cardiac Output is the full measurement of what equals a healthy amount of bloodflow. Bad cardiac output? Unhealthy amount of bloodflow. Your body's tissues and organs will suffer.
Kind of simple, but it get's the point across.

  If it helps, watch the above image for a full minute. Every time that left ventricle contracts, imagine blood is pumping to the heart and the rest of the body. Important principle, right?

CO = HR x SV

(I'm a firm believer that repetition makes things stick better, so expect to see that a lot!) 

Now, cardiac output is affected by heart rate and stroke volume. So let's break it down.

Heart Rate

If you want a more "official" definition, heart rate is the number of times the ventricles contract each minute. Normally, it's around 60 to 100. You can find that in the Iggy text on page 707.

So, heart rate is really as simple as it sounds - count the number of heart beats in a minute. Depending on the speed of your internet, the gif above should have about 60 beats per minute (bpm). There's your heart rate.

Naturally, increases in heart rate will increase myocardial (heart) tissue oxygen demand. Think of it like this: If you suddenly refused to drive your car under 100mph, you can expect your car to need more gas more often, right? Similar principle.

So, what if you were unable to get that extra gas? Let's say you drove so fast and hard you're now out in the middle of a desert. No gas station for miles and you're running on empty. You're not going to be able to continue to drive 100 mph anymore. 

Now, imagine that car is your heart - the gas is oxygen. For whatever reason, you can't take in enough oxygen to meet the needs of your heart. Your heart will at first try to compensate, but after a while we expect to see a decrease in cardiac output. And what's cardiac output again?

The full measurement of what equals a healthy bloodflow!

CO = HR x SV

Stroke Volume

Stroke volume is the amount of blood ejected by the left ventricle during each contraction (Iggy page 707). It's the difference between end-diastolic volume (the amount of blood during the relaxation and filling of the left ventricle before it contracts) and end-systolic volume (the amount of blood left after the contraction and emptying of the left ventricle).

Stroke Volume is affected by many different variable, (such as preload, afterload, and contractility) but we'll focus on Preload and Afterload for now.






Preload is the degree of myocardial fiber stretch at the end of diastole and just before contraction.


Meaning...


It measures the elasticity of the cardiac cells when the muscle fibers in the left ventricle are stretched by the volume of blood they're holding. Anatomy time!


Cardiac muscle exhibits a length-tension relationship. What that means is that resting muscle fibers in cardiac muscle are kept shorter than the defined 'optimal length' so that they are able to develop maximum tension. Therefore, stretching cardiac cells can produce dramatic increases in contractile force.


Too wordy? Yeah, it is. Here's an easier way to look at it.
Pretend the cardiac muscle fibers are rubber bands. You take a rubber band and stretch it between two fingers. Suddenly, you let it go. 

If you stretched it about this distance, it's not going to go very far, right? 

Instead, take that rubber band and stretch it with the thumb of one hand and the index finger of the other.

If you let that one go, its going to have some distance, right? Same principle with Preload. If each muscle fiber gets stretched to capacity by the filling of blood, they're going to be able to shoot the blood out to the rest of the body with enough force to perfuse all the tissues. The more the heart fills during diastole (within limits, of course) the better and more forceful the contractions will be.

Afterload is the pressure or resistance that the ventricles must overcome to eject blood through the aortic semilunar valve and into the peripheral blood vessels.

The amount of resistance is directly related to arterial blood pressure and the diameter of the blood vessels. (Iggy page 708)

So what does that mean? 

Well, your valves have to shut pretty tight. Otherwise you'll see leakage back into the atria, or blood will leak through into the aorta before the ventricles contract properly. In both instances, blood isn't going where it needs to be. What that means for the ventricles is they have to overcome the pressure that's holding the valves so tightly closed so that blood can be ejected out and go the to rest of the body - where it needs to be.

If it helps, you can picture afterload as a garden hose. There has to be enough pressure within the hose to force the water through and out. So, let's say that arterial blood pressure is represented by the hose's spigot.

The spigot puts pressure on the water, forcing it out into either a strong stream (high pressure) or tiny dribble (low pressure).

Now, let's say that the hose itself represents the blood vessels. If you've got a good clean hose, it's going to allow good water flow. If you have an old hose with mineral build up or other trash inside, that water flow is going to be restricted. Pressure may be high, but the way is blocked. Tiny blood vessels equal poor blood flow.

 So if your ventricles are having to fight against a high amount of resistance from either high arterial pressure and/or decreased blood vessel diameter, how good is your stroke volume going to be? How adequate is your cardiac output going to be?

CO = HR x SV