A normal heart pumps out 60-65% of its blood with each beat. When that fails, fluid backs up into the lungs, causing shortness of breath and a distinctive crackling sound. Treatment starts with oxygen and nitroglycerin to reduce the load on the heart, plus CPAP to help the lungs exchange gas.
Questions this video answers
Approximately 60–65%.
0.4 milligrams (400 micrograms) sublingual.
600 micrograms of nitroglycerin placed in a 50 mL normal saline bag and run (described as wide open in the lecture).
Maintain oxygenation around 88–90%.
Foreign.
We're going to talk about congestive heart failure. Congestive slash heart failure. So let's break down the pathophysiology of chf. CHF is your heart. Your heart is a pump, right? It's just a pump. It takes blood from point A to point B and making sure that the oxy, that it's oxygenated and removes CO2, right? That's all the heart does. It pumps and out, pumps and out. So when you look at that force that the heart needs, right, the what's called the ejection fraction, anywhere between 60 to 65%. That's what the normal heart function does to squeeze, squeeze, right. In congestive heart failure, that function has now been decreased.
They had a, stemming, they had a non st segment elevation. They had a infectious disease of the heart. Anything that affects the heart, that affects that function cause heart failure. So if you go down to 50%, then you have first stage of heart failure all the way to severe stage 10 to 15. Now I want everybody to understand the heart is not just to send the blood flow, but that's what give us the energy to do anything. For me to stand up right now and to be able to speak in a minute without taking a break, I need to have a normal heart function. Somebody who has limited heart function has limited activity, right? So imagine those patients, they, they have decreased pump, the blood is gonna get backed up. Remember we talked about the right side of the heart as a volume, right? So now the blood's gonna come back to the right side of the heart. It doesn't have enough force to be pushed, so it's gonna go into the lungs and it's gonna back up into your lung. And once it backs up into the lung, that's cause pulmonary edema, right? And so congestive heart failure with pulmonary edema. Now you understand the physiology. Now you just. We put the symptomology meaning the symptoms, right? Shortness of breath, right? They're tripoding, right? They can't get, they're trying to, they tripoding. They have hypertension early, right? Because their system is trying to compensate, right. For the, for the, for the lack of oxygen, the lack of function of the heart. They're going to have pulmonary edema rails everywhere, right? So this is the physiology that we need to understand. And we're going to give oxygen, but oxygen is just one treatment. What's the major important part of treating this patient? Their vascular system, their, the, the vein, right? Most of our blood supply is, is kept on the Venous side, right? We have arteries, arteries and vein, right. So the venous side is what's called the accommodating system. Most of our blood supply is always into our vein and about 2 3rd of our blood supply is going to be in the vein. Very small amount of blood is in the artery, right? The artery is a thick, thick, thick. So it doesn't accommodate for much blood in congestive heart failure. We want to cause vasodilation. Think of your tank, right? This is my tank, my blood tank. My blood tank is 6 liters, right. If I cause vasoconstriction, right. That mean I'm going to take my tank and I'm going to squeeze my tank, right? I'm going to take my six liters and make it three liters, right? I mean I'm functioning on three liters. That means a lot of blood, right. And then that's going to worsen the pulmonary edema, worsen the congestive heart failure. So what do we want to do? We want to do vasodilate. Vasodilate. We want to affect the venous part of the blood system and make it wider, wider and wider. So we take that 6 liter tank and we're going to make it 8, 9, 10 liters. All the blood now is pulled to the extremities or pulled to different part away from the heart, away from the lung. That's how we're going to treat. What medication do we have? Well, this is why we give nitro sublingual. You're giving 0.4 milligrams of nitro, that's 400 microgram of nitro. Nitroglycerin is a venodilator, Right. It's going to does exactly this affect the venous to dilate, to make the tank bigger? We're giving it sublingual. The problem with sublingual nitro is we talked about absorption, we talk about blood flow. And one of the problem sub, sublingually is the pill may not get absorbed into the because of vasoconstriction, Right? Right. It's so tight. So the blood supply in into the face may not be as delivering into the system. And so if it doesn't work, the blood pressure is systolic 160 or greater. You've given 0.8 meaning 2.4 milligram. Then we're going to go to our new protocol where now we're going to give it intravenously and understanding intravenous, you're going to take 600 microgram of nitroglycerin. You're going to put it in the 50 mic, 50 milliliter bag of normal saline and you're going to run it wide open, right? And you're going to deliver 600 microgram into the, into the venous system. This is going to go everywhere into the system. It's going to affect the entire system much faster. Something to watch. Look for the systolic blood pressure as you're running your nitro. If suddenly the blood pressure drops all the way down to like 80, 90, close it and take a deep breath. Okay? Nitro is a very short lived, lived medication. 1, 2, 3 minutes the medication will be gone and the patient blood pressure will start. Don't start panicking, don't start like oh, oh, now I got to chase it and give a fluid. You're only going to give fluid to those patients if they're not responding after five to eight minutes. When you've hold nitroglycerin simultaneously, we're going to do cpap. Right? CPAP again is continuous positive pressure, right? It's what CPAP is, it's peep, right? In event peep in a non ventilated patient. Cpap, same terminology, same, same mechanism. So what you're doing is now you're creating the negative pressure. You're going to open the alveoli to allow for more gas exchange. Not only you're going to allow for more gas exchange, but that pressure into your chest is going to allow for blood again to vasodilate. Right. And then what we want, we want the blood to be shifted and make the container wider. Right? In contrast, right? I'm going to give you a contrast, right? In patient who are trauma bleeding, right? They're bleeding, bleeding, bleeding. What's happening? The 6 liter tank is getting shorter, shorter, shorter, shorter, shorter, right? And then there's not enough force to go to the heart. That's completely opposite, right? That's what we're going to get. Fluid in chf, the tank. We want to make the tank bigger, bigger, bigger, bigger. So CPAP will increase that tank. Venodilation medication will increase that tank. Maintain oxygenation anywhere between 88 to 90%. Again, do not try to normalize a number that probably will never be normal. It can't fix a bad heart with what we have in our protocol. Most of those patients are secondary to a disease process. Either dietary indiscretion. You know they're supposed to be on 2 gram salt diet they went out to with their family and they took too much salt or they have new worsening heart disease, a new mi, a new st, non ST segment elevation, the importance of rekg, check for a new onset of infection. For looking for sepsis, surge criteria.
