Cardiogenic and Obstructive Shock

by Carlo Raj, MD

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    00:00 in Pulmonology, understand the entire system is being affected.

    00:01 Let’s take a look at the other two major shocks here. Once again, what is now causing decreased oxygenation of your tissue? We either have cardiogenic or you have obstructive.

    00:08 Let’s go through each one and the reason that these are put in the same row is because many of the features are going to be comparable and there are certain features that are absolutely distinct. So, let’s first go through cardiogenic. Obviously, the causes are going to be different, right? If it’s cardiogenic, what happened? Oh, my goodness! You or the patient has suffered a myocardial infarction. If there is myocardial infarction, one of the post MI complications include your CHF. In acute congestive heart failure, you would have then a decrease in cardiac output. You have a decrease in cardiac output. What then happens to your tissue? It’s not properly being oxygenated.

    00:48 Okay, what other issues do we have here? Acute MI, valvular dysfunction, arrhythmias. You can notice here that any one of the etiologies or differentials is all causing your heart to stop. Okay. So, if your heart stops, then what do you begin here? It’s not haemorrhaging.

    01:09 Decreased cardiac output and where does some of this fluid go? It backs up into maybe the pulmonary right, pulmonary edema. If it’s cardiogenic, it would be transudate, maybe if it’s bad enough, may result in alveolar haemorrhaging and company.

    01:24 But, decreased cardiac output. Here once again, what happens to your stretch? Decreased.

    01:28 What do you want from your medulla? You want sympathetic. Okay. So, this is example number 2 where it’s a shock. We have increase in your sympathetic and so therefore, I want you to now move into your diagnosis here and you would expect to find cold and clammy, but that’s not specific because it’s sympathetic. So, let’s go into diagnosis for each of the shocks here, cardiogenic, obstructive.

    01:57 Before we move on, I’d just make sure that we are clear about obstructive and why the heart might not be properly or the cardiovascular and the pulmonary system are not properly functioning as they should. In obstructive, cardiac tamponade, what happened here? Maybe the patient had a myocardial infarction. Maybe there was a scar formation, but it was weakened, so resulted in a ventricular aneurysm and maybe there was ventricular wall rupture. And so therefore, how quickly is this pericardial cavity being filled up? Way too quick. What do we have here? Cardiac tamponade. What is this? Obstructive type. And then we have pulmonary embolism. Pulmonary embolism would also be considered an obstructive type. Let’s talk about the diagnosis. So, apart from the cold and clammy, because of why? Sympathetic. Let’s talk about congestive heart failure. In CHF, well, what’s that heart sound that you’re going to create when you have a very large left ventricle? Take a look at the chest X-ray and you find your PMI, your point of maximum impulse to be laterally displaced, by the midaxillary.

    03:03 That’s a very large left ventricle and so now, at this point, as soon as you have diastole early on, this mitral valve opens and, blood rushes into left ventricle creating S3. Where is S3 in relation to S1 and S2? Good. After S2. So, S2 would be the closure of the aortic and right after closure, you’re going to open up your mitral valve and you’re going to create, massive flow of blood from left atrium into left ventricle creating your S3 gallop. Hopefully, that’s clear.

    03:38 Next, well, say that your heart’s not functioning properly. You’re going to back up. Where? Lungs. One side or two sides? Both sides. With what? Good. Pulmonary edema. On your X-ray, you’d find bibasal type of opacity and upon auscultation, crackles.

    04:00 It’s a bibasal crackle. Number 1. If it’s the right side that’s affected, then you’re going to have, what’s this right here when your internal jugular vein can be seen to be pulsating? You should never normally be able to see the internal jugular vein, but if you find it to be pulsating, that's your positive JVP, jugular venous pulse.

    04:22 Are we clear? Heart issues, cardiogenic. Okay.

    04:27 What about obstructive and company? Here you might have tracheal deviation with obstructive, especially something like cardiac tamponade and here, because it’s obstructive, well, if your pericardial cavity is being filled up, you cannot properly hear your heart sounds. And so therefore, it will be muffled. Okay, now, my problem is this. Now, don’t memorise this. Work with me. The heart isn’t working properly and if it’s congestive heart failure, which is the best example to give you at this point? And then you know the heart is filled with blood, the volume overload. And so therefore, there’s more blood in your heart, isn’t it, in CHF? And so therefore, this is then referred to as being preload. You expect your pulmonary capillary wedge pressure or your central venous pressure to be increased and that’s what you’re seeing here, an increase in preload. Next, well, here, if your heart’s not working, either obstructive or cardiogenic, you can expect your cardiac output to be, decreased severely. And, what kind of symptoms are you finding here? The type of signs, cold and clammy, right? Sympathetic nervous system, what is that then doing to your systemic vascular resistance and arterioles? Good. Vasoconstriction, increase in TPR. Now, would treatment obviously be different? If it’s congestive heart failure and you’re trying to re-establish your pumping motion, then obviously you want to use a positive inotropic agent, maybe something like Dobutamine, a Beta-1 agonist. And if you want to try to take care of that edema, now you’re thinking about? Good. Furosemide, a diuretic.

    06:01 Whereas if you are dealing with obstruction, if it’s obstruction that you’re dealing with, then you’re thinking about relieving the obstruction. And if you want to relieve the obstruction and it’s a PE (pulmonary embolism), you want to blast open that clot and then if it is something like cardiac tamponade, what do you want to do? Open up a window ASAP so that you can drain that fluid and this is then called Pericardiocentesis.

    06:26 The last step that we’ll take a look at, as far as shock where the cardio and the pulmonary

    About the Lecture

    The lecture Cardiogenic and Obstructive Shock by Carlo Raj, MD is from the course Pulmonary Critical Care.

    Included Quiz Questions

    1. Glossopharyngeal nerve.
    2. Recurrent laryngeal nerve.
    3. Trigeminal nerve.
    4. Hypoglossal nerve.
    5. Vestibulocochlear nerve.
    1. Increased sympathetic outflow.
    2. Increased baroreceptor firing.
    3. Decreased afterload.
    4. Increased preload.
    5. Increased cardiac output.
    1. Patient with severe pancreatitis and massive ascites.
    2. Patient with massive blood loss from gun shot wound.
    3. Patient with congestive heart failure.
    4. Patient who is severely dehydrated.
    5. Patient with uterine haemorrhaging after childbirth.
    1. 0.9% normal saline
    2. 0.45% normal saline
    3. Fresh frozen plasma
    4. Albumin
    5. D5W
    1. Pulmonary capillary wedge pressure.
    2. Central venous pressure.
    3. Mixed venous O2.
    4. Diastolic blood pressure.
    5. Total peripheral resistance.
    1. Decreased afterload.
    2. Magnitude of decrease in cardiac output.
    3. Low cardiac output.
    4. Increased pulmonary capillary wedge pressure.
    5. Increased afterload.
    1. S3 gallop
    2. Warm skin
    3. Muffled heart sounds
    4. Unilateral crackles
    5. Anhydrosis
    1. Cardiac tamponade
    2. Pulmonary embolism
    3. Congestive heart failure
    4. Acute Myocardial infarction
    5. Arrhythmia
    1. Furosemide
    2. Angiotensin II antagonist
    3. Angiotensin receptor blocker
    4. Beta blocker
    5. Dopamine

    Author of lecture Cardiogenic and Obstructive Shock

     Carlo Raj, MD

    Carlo Raj, MD

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