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Shock is a condition in which the cardiovascular system fails to support the body’s basic metabolic needs. The basic systemic effects revolve primarily around vital signs. Shock causes in tachycardia. In the vast majority that’s true. However, as the heart sometimes fails, the response is bradycardia. That can result in hypotension and all of the other symptoms of shock. In patients, especially younger patients, who are dying from hypoxia or respiratory problems, frequently will present as a bradycardic rhythm in the late stages. When you see that in a child, it usually isn’t a primary heart problem. It’s usually a
Hypotension is very frequently synonymous with the concept of shock. Hypotension or low blood pressure is basically the way that we look at a patient in shock. It’s because that is the best monitor we have of how well the patient is being perfused. Obviously, hypotension and perfusion are two different things. What we’d really like to know is how well organs are being perfused. But we really don’t have good measurements of perfusion in the un-monitored patient and what we try to rely on is a patient’s blood pressure to determine how severe the shock state is. Now when you are talking about hypotension as being synonymous with
Another thing that frequently enters into it, vital sign-wise, is looking at the respiratory rate. Most patients who are hypotensive and tachycardic also become tachypneic. That’s primarily a response to the metabolic acidosis that results from the shock state. In other words, poor perfusion resulting in changing of your respiratory type resulting in release of fixed acids which stimulates the respiratory tree to increase the respiratory rate. So when you see tachycardia, hypotension and tachypnea that is one of the more classic descriptions of the shock state. What we then do is add the vital signs to various other - what I refer to as - output
The other thing that we tend to pay attention to when you are dealing with the hypotensive, tachypneic, tachycardic patient is the stimulation of compensatory responses. As a matter of fact, many of you of my age were taught to recognize shock based on these compensatory changes. Aside from the vital signs, you see
The other thing that we tend to think about also are some of the hormonal responses. Epinephrine, norepinephrine being the classic examples of some of the hormonal responses. Not only do they cause vasoconstriction but they also cause the tachycardia. When these responses are blocked - as we are doing to many
When you clinically assess a patient in shock, I spend a lot of time actually looking at the periphery and looking at some of these compensatory changes. Here’s an example of myself examining a patient who is clinically in shock. This is a patient who actually at this time had a blood pressure in the 60’s who was dying from
So the general assessment should include the vital signs, the skin vitals, basic ABC’s of how the patients is responding, what the level of consciousness of the individual is, and what their neurologic assessment it. These two can be somewhat different. By level of consciousness I mean their mental status, and by
While you are thinking, also interceding in the disease process is important. I don’t spend a whole lot of time worrying about why my patient is in shock. I spend a lot of time doing the basic stuff. I’m a surgeon and I tend to approach things in the primary process. And when I’m approaching a patient in shock what I’m doing is providing oxygen for the patient, making sure the patient is breathing adequately, does the patient need augmented respiration? Does the patient need to be intubated? What can I do to support the circulation? Should I cram in some IV’s and start some fluid on the patient? Hopefully by that time I have woken up and I
From the standpoint of the heart, cardiogenic shock is one of the major forms of shock types that you as clinicians deal with on a regular basis. Fortunately I don’t deal with it as frequently as a surgeon, however I do see it from time to time. The other day I just finished fixing a guy’s liver after he fractured his liver, and the patient got up to the intensive care unit and the patient was hypotensive, tachycardic and of course I had left the operating room and was heading home - this was
Pericardial centesis is the medical treatment of choice when somebody develops a pericardial tamponade, pressure around the heart. It is less commonly utilized in somebody who develops acute tamponade from a gunshot wound or a stab wound. Se tend to open the chest and then fix the hole in the heart. But again, this process with decrease the amount of blood building up around the heart and hopefully decrease the pressure around the heart, and hence elevate the blood pressure, decrease the tachycardia and alleviate the problem. As I said, this was a temporizing process for the majority of things that I deal with, but occasionally it can be a definitive treatment for somebody with uremic effusions that are interfering with the mechanical activity of the heart.
The kind of shock that we tend to think of - and I think classically, from the 30’s - we have always defined shock as hypotension from hypovolemia from the original studies of Wiggers et al in the 30’s. We began to realize that the fluid in the vascular system had something to do with your blood pressure and if you drained somebody of their blood they tended to get hypotensive. Since that time we have sort of reinforced those concepts. I think all of us are pretty much tuned into the fact that one of the first things you need to do in a shocky patient is usually give them fluid. The only exception being, of course, those patients that have evidence of pulmonary edema. For the most part volume loss you see with patients with trauma, burns, fractures and the medical patients with fluid loss,
If you take two to three units of blood out of a patient, these patients begin clinically
to look a little bit different. They are a little bit anxious. They may be a little vasoconstricted. Their respiration’s go up to 20, maybe a little bit more. Their pulse is greater than 100. Their urinary output begins to decrease, but still it’s not too bad. Look at this. The blood pressure is still the same. Blood pressure really isn’t a great gauge of blood loss. Here we have 1500 ml of blood taken out of this guy that has 5 liters of blood on board, and the blood pressure is still normal after removing that much. If any of you have ever seen 1500 ml of blood on the floor - and I see it from time to time, usually in the operating room - what that means is
Once you get above that value of 1500, patients start looking sick. These are the classic patients. Their respiratory rate is high, their pulse is high. They have minimal urinary output, they are vasoconstricted so their capillary blanch test is positive; it stays white. When you press on it it’s white and when you let go it’s white and it doesn’t get better. Their blood pressure now is decreasing usually to less than 100 in a standard size adult. Their pulse pressure is such that the nurses frequently record a systolic, but they don’t necessarily record a diastolic because they can’t hear it. The patient begins to get confused and anxious. When you
Another form of shock, septic shock. We kind of define shock in two types. You have low output septic shock and high output septic shock. For the most part low output is what it sounds like. Patients actually have a low blood pressure, they are not vasodilated - in fact they may be vasoconstricted. The source of sepsis is very frequently not gram negatives, maybe gram positives. There are a lot of mediators that are released in this type of patient that tend to promote this vasoconstriction and probably also has direct effects on the cardiac activity. The treatment of low output septic shock is again volume restoration, control of
Some of the mediators that have been associated with the septic syndrome. One is cachectin or tumor necrosis factor. This is released as a response to bacterial lipopolysaccharide, the bacterial cell wall. The primary source; it’s produced in a mononuclear phagocyte and basically what it does is it activates the inflammatory neutrophils and monocytes, so it actually has a positive benefit to an organism. It also activates the development of some other inflammatory cytokines which help
Another example is the interleukin pathway there - I think there’s 18 or 20 of them now. These share many of the functions of tumor necrosis factor. They are produced by the activation of the monocyte. They activate also some of the prostaglandin pathways. So here we have a cytokine that’s involved in the activation of some of the thromboxane’s and the prostacyclin’s of the prostaglandin pathway which causes local vasoconstriction and vasodilation. It also stimulates other interleukins. There have also been a number of different tests that have looked at antagonizing these molecules to determine if you can lessen the effects of the sepsis syndrome, and many of these are still in study now.
Another form of shock is neurogenic shock. Now neurogenic shock, in my business as a trauma doctor, is basically high spinal cord injury. Remember that the cervical sympathetics actually control vasoconstriction in a patient. So if you take out a patient’s spinal cord at a high cervical level, what that does is it makes a patient not respond to epinephrine in the usual fashion, and norepinephrine. In other words, their cervical sympathetics are gone, they do not vasoconstrict in response to shock and they do not become tachycardic. In other words, they do not respond to the nervous stimulation of the sympathetic nervous system. So what you see is a patient who is in shock but isn’t tachycardic; is actually either normocardic or bradycardic and has peripheral vasodilation. When you start
Here’s an example of one of those patients. This is a cervical spine series and you can see there’s one, two, three, four, five, six, seven cervical vertebrae here. But remember, what you want to see is C7 and the top of T1. The reason you want to do that is because here’s C7 now and you see here’s T1 over here and essentially what this individual has done is sliced their cord at that level due to this subluxation. Now in an awake patient who can respond to you and you can
Hormone increases in shock. This is one of those board questions that people always ask, so I throw these slides in. There are a number of hormones that are released in the shock state and basically they are the stress hormones; ACTH, cortisol, renin, aldosterone, epinephrine, norepinephrine, vasopressin, growth
So what do we do to the patient in shock? The basic thing is a physical exam. A physical exam will tell you roughly, does the patient have compressive shock? Does the patient have hypovolemic shock? Does the patient have neurogenic shock? Cardiogenic shock? A good physical exam can usually differentiate all those
We also should consider the need for invasive monitoring. Patients that are sick may need to be monitored closely. In this day and age, that’s not as common - the invasive monitors - are not as commonly used as we use to in the past and I think that’s because we are better clinicians now. We also now have a lot better non-invasive monitors. When you have your choice between a good non-invasive monitor and a good invasive monitor, you should always pick the non-invasive
Now the use of vasoreactive agents - and I’m talking about vasodilators, vasoconstrictors, contractility agents - should be reserved for those patients that will benefit from them. The vast majority of patients require volume resuscitation and then once they are adequately volume resuscitated - and how do