----start----- surg 10.28.97 Dr. Cynthia Otto shock in small animals There was a handout given a while ago "shock in small animals" The main thing - what is it,how do you recognize it? slide: dog in shock shock is "any condition that leads to poor perfusion of the tissues" the most important thing is what happens at tissues - not getting oxygen, glucose, other nutrients, and there is buildup of byproducts of metabolism. effect: cells/organs not getting essential nutrients and toxins accumulate treatment: improve perfusion kinds of shock: hypovolemic distributive cardiogenic when talking about the patients you have in surgery, any kind of shock can occur as a complication, or might be an indication for surgery. hypovolemic shock can occur due to a lot of bleeding in surgery, or due to trauma. not only blood loss but fluid loss ie from vomiting or something, can cause hypovolemic shock. also, animals with third space problem - fluid accumulation in intestines, or other body cavities - ascites, etc - can't absorb fluid into circulation so are effectively hypovolemic w/hypovolemic shock, animal is very pale, heart is normal, there just isn't enough blood to go around. distributive shock - not limited to septic shock. neurogenic problems, anaphylaxis, or certain drugs can cause this type of shock in which all blood vessels dilate. Normal heart, but increased volume of circulatory system, so despite normal fluid volume, there is an effective hypovolemia due to dilation of blood vessels and not having enough blood to fill up all the vessels now that they're bigger. cardiogenic shock: most different. this is actually pump failure. treatment is very different. the heart is the primary problem. treatment of the other types of shock is to increase the volume. but when the heart already can't handle the load and you pump in volume you make it worse. so you have to differentiate this. this is caused by heart failure, arrhythmias, pericardial effusion, or tension pneumothorax. IN your patients, you might have an animal with normal heart function but when you put it under anesthesia, you push it into cardiogenic shock. this is the only type of shock where the heart itself is the problem. heart can't get enough volume into circulation. these animals also look pale. how to tell them apart? pulse quality, pulse rate - probably high in both cardiogenic and distributive shock. how else can you tell them apart? if there is an arrhythmia. the history also might be helpful - hx of trauma? hx of heart dz? how does the body respond to shock? it's a precarious situation. the response is only a temporary, stopgap solution. there are sensors in the macula densa checking sodium delivery, and there are afferent stretch sensors which respond to hypovolemia. also pressure and chemoreceptors in aortic arch and carotid body. primary problem is poor perfusion so the body will increase respirations then will try to increase perfusion dilated cardiomyopathy - will cause cardiogenic shock - dog pale, tachypneic what do you do? you can supplement with oxygen or ventilate for them. treatment to augment increase in O2 - supplement O2 - how? hold hose in front of face, use oxygen cage, use nasal oxygen cannula. also to improve oxygen delivery - improve perfusion - improve circulation. if there is still big trouble, you may have to ventilate the patient but this is usually only when lungs are affected. slide: dog shot in the mouth. he's in hypovolemic shock. we need to increase perfusion. we need to provide volume. how? body normally responds by increasing cardiac output - increases HR since can't increase stroke volume. these animals are tachycardic. what's tachycardic? well, normal is about 60-160. if over 160, something is probably going on. why is the HR increased? in these cases, because of poor perfusion. If hypovolemic or distributive shock, need to give volume. If cardiogenic, need to fix heart! so you increase CO - let the body take care of increasing HR. Then, you work to increase SV - by giving more fluids. You don't want to further increase the HR as part of tx because then you will be decreasing SV because heart won't fully fill. During the filling phase, (note that as HR increases, diastole is shortened - diastole is filling phase) the perfusion of the heart occurs. if you decrease diastole, you decrease time of coronary perfusion. and a heart working faster needs more blood, not less! increasing HR temporarily will increase perfusion and O2 delivery but it increases demands on the heart, and decreases perfusion of heart. so if you don't treat hypovolemic or distributive shock, you can end up with heart failure. how does the HR and contractility normally increase? sympathetic drive and catecholamines - huge release of these in any form of shock. this is b/c kidney and stretch receptors respond and initiate this kind of response. what about treatment to increase SV? how? fluid therapy, to increase circulating volume. this is the mainstay of tx for hypovolemic and distributive shock. not cardiogenic shock. another thing the body does is to cause really strong vasoconstrictors - these come from kidney - cause more blood to return to the heart. but we should not work to constric things more than the body normally will. if you do, you will make things worse. You will end up with the "low men on totem pole" eg intestines, skin, not being perfused. people look cold, clammy, blue tinged due to this constriction. intestine gets the same way - but there are alot of bacteria in the intestine,and if there is poor perfusion to intestine, you can break down barrier against bacteria, and bacteria might move into blood and cause sepsis. so, hypovolemic shock can lead to cardiogenic and septic shock. so we don't increase vasoconstriction unless we've drastically increased volume already. increase in SV - vasoconstriction, the body's normal response, will increase venous return. we use that to help recognize shock. this is obvious b/c animals are pale, cold limbs, decreased rectal temp. then we ourselves can increase intravascular volume, b/c the body can't do that acutely - the body increases salt and water retention, but that is a more chronic mechanism. what about the energy needs? you have to increase nutrients. you must be sure to maintain the blood glucose and provide nutrition if this goes on for any length of time. normal response of the body: aldosterone release from kidney -> salt and water retention, vasoconstriction growth hormone glucocorticoids -> increase glucose available, gluconeogenesis, enhance catechole response. there is this distributive shock we've discussed. all the pathophysiology we discussed so far is generalized, occurs in all forms of shock...but septic shock has some additional things to know about. in septic shock, the immune system is stimulated. usually the reason this occurs is bacteria or endotoxin (LPS). that response of the immune system is essential to control infection but when it gets out of control it creates generalized inflammation throughout the whole body. imagine cat abscess - local inflammation. think about what happens if that were everywhere in the whole body. whole thing goes up in flames. SIRS: systemic inflammatory response syndrome - describes what happens in patients when there is this huge out of control immune response. this response can also happen in the absence of infection! if we see something that looks like septic shock in the absence of infection we can just call it SIRS, whereas septic shock is similar but is caused by bacteria. risk factors for SIRS: trauma. tissue injury will initiate an immune response so dead/injured tissue is cleaned up. if injuries are very severe you can get sirs. immunosuppression can do the same thing. hypotension can also do the same thing - remember about intestine needing good perfusion so that it can be a barrier to bacteria - bacteria can move into the circulation and initiate the immune response. actually, even without bacteria moving in, low perfusion on its own can initiate this immune response just due to tissue injury. so realize that SIRS is an umbrella term. how is septic shock different from hypovolemic shock? partly pathophysiology. when immune system is stimulated there is cytokine release. cytokines trigger responses in other immune cells/endothelial cells. if you take away cytokines you die from infection. but when this becomes a systemic release you see adverse effects - it activates all the endothelium causing vascular leakiness, edema, fluid loss from blood vessels, interfering with organ function, etc. also you get activation of clotting in a disseminated manner - DIC - and the cytokines are part of the reason this happens. there are also vasoactive products eg NO triggered by cytokines. NO important in normal vasodilation, but when you make lots of it you can see profound vasodilation. normally w/shock you get vasoconstriction. so this vasodilation is a huge difference between septic/distributive shock and hypovolemic shock. these patients are red, not pale. then you also activate PMNs and mphages as well. trauma/inflammation can stimulate hypotension or ischemia/reperfusion injury. then bacterial translocation can occur, but isn't fully necessary. you get stimulation of cytokines, SIRS and or MODS - multiple organ dysfunction syndrome - all organs including vascular start to fail, and you end up with dead patient. this is a very serious condition. the recovery rate is very poor. once patient goes into SIRS/MODS, chance of bringing patient back is very slim. signs of hypovolemic shock: pale mms prolonged CRT temperature normal or decreased due to lack of perfusion of rectum. signs of septic shock: bright red mms CRT rapid - these patients are hyperdynamic temperature increased or decreased. may be febrile or very subnormal both septic and hypovolemic shock produce: tachycardia - over 160 in dogs, over 220 in cats pulses - bounding early, weak late. nutritional response - we talked about stress response, catecholamines in SIRS/sepsis - early on you get hyperglycemia, later you see hypoglycemia, b/c cytokines interfere with glucose metabolism, cause increased glucose consumption. in hypovolemic or cardiogenic shock, will be normal or mildly hyperglycemic normal around 90-110. so we may see up to 130, 140. we might also see clinically, as things progress, perfusion to brain is eventually compromised plus there are circulating factors that may lead to mental depression, and you will also see decreased urine output due to kidney trying to maintain salt/water or due to lack of perfusion of kidney. these signs are seen with SIRS/Sepsis and with hypovolemic shock. lab findings - there will be acidosis with both hypovolemia and SIRS. why is that? the respiratory component is negligible. the acidosis comes from lactic acid - poor perfusion, lactic acidosis occurs from anaerobic metabolism. how about glucose? normal/sl increase with hypovolemic shock, and decreased with SIRS. usually the hyperglycemia with SIRS is too early and you don't see it. the hypoglycemia is profound with these cases. PCV - increased (if there is pure water loss, eg from vomiting) or decreased (from blood loss) with hypovolemia, decreased with SIRS TS: if there is pure water loss, the TS will be increased - eg if there has been hemoconcetration from severe vomiting, in hypovolemic shock. but generally decreased in both cases. in SIRS, can see both values low, or both normal. how do you treat? the key is VOLUME for hypovolemia/distributive shock. cardiogenic shock: the key is pump support. fluid therapy: give shock dose of fluids - 90 ml/kg to effect. you can't just say that it's 90 ml/kg/hr because you have to do it to effect. the problem with this is we have to think about it. is the animal in shock? If yes, dogs get 90 ml/kg cats get 60 ml/kg given to effect. you start off with some, and you watch the HR - is it starting to slow down, suggesting increased perfusion? are mms looking better? those signs help to guide the fluid rate. some dogs need more, some need less. it's all going to be to effect. what fluids will you give? there are different kinds. there are colloids, which hold water in the vessels. blood is a colloid. hetastarch, hespan, dextran. generally, we start with crystalloids. they are cheap, available, and usually work ok. in animals suffering with hypovolemia due to hemorrhage, you need to think about giving blood also. which crystalloid do you give? normosol R, LRS, 0.9 % NaCl, 5% dextrose? LRS and NaCl are ok. Dextrose in water is bad - is hypotonic once it's in the body due to glucose entering cells. do NOT use this for resuicitation. ever. saline pH is acidic - pH 5. LRS pH 7.4. remember this! so you wanna use LRS because your animal is already acidotic. if you use a colloid, divide dose by three, because it will stay in vessels. give fluids fast. is animal dehydrated? if yes, what %? multiply % by wt in kg. that is the number of liters to rehydrate them. guide to % dehydration 5-7 min detectable 12-15% close to dead. if acute, replace more quickly, if chronic, more slowly. if not eating/drinking, consider maintenance fluids. vomiting, diarrhea, fever, burns, wounds ->ongoing losses fluid therapy chart in notes: flow chart. check it out. figure shockdose, rehydration dose, maintenance, and ongoing losses. you calculate it, start giving it, and monitor patient to make sure dose is appropriate. if patient is getting worse or not improving, reevaluate!!!! ----end-----