SHOCK: 1. DEFINITIONS & DETERMINATIONS
What is Shock?
- Fundamentally, shock is a mismatch between oxygen supply and oxygen demand.
- Shock is really measured at the tissue level. So shock occurs when individual tissues in the body receive inadequate oxygen supply to support their metabolic needs.
- Shock is often associated with hypertension. It’s not the same thing as hypotension. It’s possible to be hypotensive without being in shock and it’s also possible to have shock without hypotension.
What is Oxygen Delivery Determined by?
- Oxygen delivery is the primary determinant of the shock state. How much oxygen your lungs and your blood are able to deliver to your tissue is what determines whether or not your tissue is hypoxic and whether or not you are in shock.
- So, what determines oxygen delivery? Very simply, it’s cardiac output and arterial oxygen content. So the delivery of oxygen is determined by your cardiac output times your arterial oxygen content.
What is Cardiac Output Determined by?
- Well, as you may remember from physiology, cardiac output is your heart rate times your stroke volume.
- CO = HR x SV
- It’s a classic physiology equation.
- So your heart rate and your stroke volume determine how much blood your heart is sending out to the body.
What is Stroke Volume Determined by?
- Preload is a major determinant. So that’s how much volume is in the ventricle at the end of diastole. How full the ventricle is.
- Myocardial contractility, that’s how hard the ventricle squeezes to push that blood out to the body.
- And then afterload, which is how much resistance the heart has to work against in order to send blood forward through the system.
Preload and Stroke Volume
- These two things are really closely related to one another.
- And regardless of your contractility, regardless of how effectively the heart is working, the Frank-Starling Law tells us that stroke volume increases as your preload increases. So as you increase the amount of blood in the heart at the end of diastole you’re gonna actually increase the amount of blood that the heart sends out to the body.
- Now, that’s only up to a point. You can’t just put endless amounts of fluids into people and grossly distend the ventricle and expect it to squeeze harder, but up to a reasonable physiologic level the ventricle will give you more output for the more preload you have.
What Arterial Oxygen content determined by?
- Well, very simply, that’s the oxygen saturation which is generated by the lungs and the amount of hemoglobin that’s in the blood.
- So your hemoglobin binds to your oxygen and that’s how oxygen is delivered to tissues, so you need to have an adequate hemoglobin concentration and you need to have adequate lung function to saturate all of that hemoglobin.
- So arterial oxygen content is hemoglobin times arterial oxygen saturation.
- Let’s just review what we’ve talked about physiologically. So delivery of oxygen to tissue is what determines whether or not you’re in a shock state that is determined by cardiac output and arterial oxygen content.
- Cardiac output is your stroke volume times your heart rate.
- Whereas arterial oxygen content is your hemoglobin times your saturation.
- Stroke volume is influenced by preload, contractility and afterload which are all physiologic parameters that you as a physician can manipulate to help your patient.
- And oxygen saturation is determined by your airway and breathing status which again are physiologic parameters that we can manipulate to assist our patients.
SHOCK: 2. TYPES & CLINICAL MANIFESTATIONS
Types of Shock
Not all shocks are created equal and there are a number of different physiological arrangements that all end in the same final common pathway of clinical shock.
Cardiogenic shock is the first one we’re gonna look at and in some ways, it’s the easiest to understand.
- In Cardiogenic shock, you have acute impairment of cardiac output for one reason or another. It’s most commonly associated with coronary syndromes. You have a massive MI and you’ve infarct a large amount of you myocardium. You can imagine that infarcted myocardium isn’t gonna squeeze anymore. So instead of having a nice rigorous contraction with every beat of the heart, you now have a very weakened ineffective contraction with every beat of the heart which of course is gonna impair your stroke volume and ultimately impair your cardiac output.
- There are other conditions that can do this though, various drugs and toxins, of course cardiomyopathies will have the same effect, valvular diseases can potentially render your cardiac contractions ineffective. And dysrhythmias can also impair filling time and decrease the effectiveness of cardiac output. So there’s a lot of conditions that can lead to cardiogenic shock, but they all have the common end result of pump failure, i.e Reducing the ability of the heart to contract effectively.
Hypovolemic shock is also pretty easy to understand. That’s all about preload.
- So basically if your blood volume is on the floor instead of inside of you vasculature that’s obviously gonna reduce your preload. You’re not gonna have blood in the vessels to put into the heart during diastole, so your cardiac output is gonna be impaired.
- Now, your body will try to compensate for that by raising the heart rate and by clamping down on the vasculature, raising the systemic vascular resistance. These are normal physiologic compensatory mechanisms to try to maintain perfusion at the tissue level.
- However, the disease process is fundamentally all about preload, and as you can imagine it’s gonna be treated with agents that will bring your preload back up, namely fluids or blood.
Distributive shock is a form of shock where all your blood is inside of the vasculature where it belongs, but it’s maldistributed.
- Your vasculature is dilated, and boggy and has poor tone and instead of effectively delivering blood to tissue, you now have vasodilation in the periphery which causes blood to just kind of hang around not getting where it supposed to go.
- We see this particularly in sepsis and anaphylaxis and the physiologic effect primarily is loss of systemic vascular resistance. You’re vasodilated and you’re not gonna be able to effectively distribute blood to tissues.
- However, in distributive shock there is some direct myocardial effect as well, and that’s important to remember. Your body will try to compensate for this by raising the heart rate but that usually only works to a certain extent. So you’re not gonna get full physiologic compensation.
The last form of shock is obstructive shock.
- These are the conditions where there some sort of extra cardiac blockage to blood flow that prevents the heart from filling normally.
- So in cardiac tamponade there’s a pericardial fluid or blood collection that mechanically compresses the heart and prevents it from filling.
- In tension pneumothorax there’s gonna be a big hight pressure air collection in the chest that again compresses the mediastinum prevents normal cardiac filling, actually prevents normal venous return back up into the chest by making the intrathoracic pressure positive.
- Pulmonary embolism, well, very simply, if you’ve got obstruction to flow on the right side of the heart, you’ve got a big clot that’s prevents the blood from circulating out of the right heart, and through the pulmonary vasculature, you’re gonna have impaired input on the left,. You’re not gonna be able to fill the heart adequately and send blood out to the body.
- So these are also diseases of preload much like hypovolemic shock, but they’re all conditions where the problem is obstruction of normal blood flow and maldistribution of blood rather than blood loss.
Clinical Manifestations of Shock
What is shock look like clinically?
- Well, as you can imagine it very commonly is gonna involve tachycardia because as your cardiac output drops, your heart is gonna try to compensate for that by increasing rate. That’s a normal physiologic compensatory response to impaired profusion. When the heart is not putting out enough blood to meet the physiologic needs, the sympathetic nervous system will tell it, “beat faster, beat harder.” So you see tachycardia in this settings.
- You’ll also very commonly see tachypnea, so as the tissues become hypoxic, a normal physiologic compensation for that is to try to breathe more and get more oxygen into the blood in order to provide oxygen at the tissue level. So it’s not uncommon to see patients breathing quickly and in some cases even to see respiratory distress.
- You’ll often, but not always see hypotension, so as you can imagine in many of the shock states that I described were either your blood volume is missing entirely or it’s not being circulated appropriately to the body, because of pump failure or vasodilation, you might see an overall reduction in blood pressure.
- Now, one thing I wanna make sure to remind you about is that’s not always gonna be absolute hypotension. Generally in a healthy person, you will see numbers that are reflective of true hypotension. But if it’s a patient who’s chronically hypertensive and they’re running around with the systolic of 160 or 170 their entire lives they might be significantly hypotensive at 120. So you wanna make sure that you’re always thinking about your patient relative to their baseline rather than just the absolute numbers that we learned in medical school.
- Altered mental status is a common manifestation of shock, because the brain is extremely sensitive to tissue level hypoxia, and if you’re not delivering adequate oxygen to the brain, it’s not gonna work properly.
- We also see oliguria or anuria when you’re not adequately profusing and oxygenating the kidneys.
- You might see pallor or cyanosis which is reflective of the global hypoperfusion of the patient.
- You might see cool or mottled extremities again, reflecting shunting of blood away from the periphery and toward the vital organs which is a normal physiologic compensation for shock.
- And you might find faint peripheral pulses. Again because the body is trying to shunt blood centrally and maintain blood flow to vital organs, so you’re gonna loose blood flow out in the periphery where you would normally have it in a nonshock state.
- Bottom-line, is presentation of shock is gonna be highly variable based on what the underlying causes. What’s going on with the patient? And also how well compensated the patient is.
You can see patients in shock who look remarkably well. And you can see patients in shock where one step away from cardiac arrest. And you really got a range anywhere in between. So you always wanna think about what your patient’s personal baseline, physiologic status and how different they are from that. And remember there’s gonna be a lot of variability in what patients in shock look like clinically.
Shock: 3) General Management
General Management of Shock
- So in terms of general management, You know, we discussed earlier how shock is a disease of tissue-level hypoxia. So we wanna be really attentive to airway and breathing for these patients. Everybody should get supplemental oxygen no matter what.
- Shock is also a disease of circulation, so we wanna make sure that everybody has adequate IV access and once again, that is two large-bore IVs. We wanna make sure we can give high volume fluid resuscitation if we need to.
- We wanna also, always consider a fluid challenge in shock. Now, not every patient is gonna benefit from fluids. As you can imagine in cardiogenic shock when your problem is really lack of cardiac squeeze. You know, increasing the amount of circulating volume isn’t gonna do you a heck of a lot of good because these patients aren’t typically coming in hypovolemic. However, in most other causes of shock, filling up the tank is a really good idea and might produce some clinical benefit for your patient.
- But the most important thing to think about in shock is what’s causing it and how can I reverse that underlying disease process.
Shock is all about the ABC’s.
Let’s start off with A and B and just remind you why airway and breathing are so important.
- So again, we wanna give supplemental oxygen to get a saturation of 95% or greater. Now, if your patient has pulmonary disease, they might be okay at 92, 93 but we definitely wanna raise the oxygen saturation up to a physiologic level for that patient because this is a disease of hypoxia. So we wanna make sure that their saturation is adequate, making their arterial oxygen content adequate to ultimately allow them to deliver oxygen to tissues.
- Now for most patients, simple supplemental oxygen is gonna be fine, but if your patient has really severe shock or if they have significant respiratory distress, you might need to think about intubation in order to decrease their metabolic work of breathing and enable them to optimize their oxygenation. So, the amount of intervention you’re gonna need for airway and breathing is gonna vary based on the patient’s clinical status.
Let’s move on now to C.
So we always wanna think about fluid resuscitation for our patients in shock.
- Like we discussed before, IV fluids increase preload. When I increase my circulating blood volume I’m gonna increase the amount of blood that’s in the ventricle at the end of diastole which according to the Frank-Starling Law, is gonna then increase my stroke volume which in turn increases my cardiac output, ultimately allowing me to better deliver oxygen to tissues. So, this is really all about the physiology. When I optimize my preload, I optimize my cardiac output and I do a better job getting oxygen where it needs to be at the tissue level.\
- For vascular access which is also part of C, remember we wanna make sure that we’re able to give large volumes of fluids if it’s necessary.
- So that means we need to minimize resistance to flow through whatever vascular access devices we use. So we want large diameter devices that are short as possible. We all remember Poiseuille’s law which tells us the radius of a tube is the biggest determinant to how quickly fluid can flow through it.
- So a big diameter tube is gonna let us give a lot of fluids quickly and a short tube is gonna let us give a lot of fluids quickly which is why peripheral IVs are really better than central venous access devices.
- Although of course, if you’re not able to get adequate peripheral IV access you will need to place a central line. You’re just gonna wanna use the largest caliber one you can get your hands on.
When we give fluid, we’re always gonna start off with isotonic crystalloid by which I mean normal saline or lactated ringers. However, we don’t wanna be giving fluid indefinitely.
At some point, if the patient is bleeding or has significant anemia, we’re gonna wanna think about switching over from crystalloid to blood products. Consider transfusion in patients and whom it’s indicated based on their either clinical bleeding status or their laboratory-measured hemoglobin.
The amount of volume that you have to give is gonna vary according to what’s going on with the patient.
So if it’s a patient in a hemorrhagic shock who has a major bleeding source, they might need litres of fluid and units and units of blood in order to maintain their circulating volume.
However, if it’s a patient who has a mild myocardial infarction and they started off pretty much euvolemic, you might not need to give them any fluid or only a very small amount.
So you always wanna make sure that you’re reassessing your patient frequently while you’re giving fluid or blood, that you’re considering their underlying physiologic state and their comorbidities, and you’re using their response to treatment to guide how you continue with their resuscitation.
Points to remember
- So, bottom-line take-home points about shock is you can always think about shock as tissue level hypoxia and when you think through that physiology, it’s gonna point you in the right direction at the ABC interventions that you need to perform to get a patient out of shock.
- There are lots of different disease states that can cause shock and the presentation of shock clinically is gonna vary based on what caused it and how well-compensated the patient is.
- Initial treatment is all about the ABCs so that’s gonna involve supplemental oxygen and airway management if it’s necessary, also intravenous fluids and potentially blood products.
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