Shock, Sepsis, Sirs, Mods Flashcards
1
Q
What a shock?
A
Not enough oxygen for tissue perfusion.
2
Q
That is really the essence of shock one so when you watch TV and you watched all of the medical dramas, and the patients are in shock, what are they treating them with?
A
Fluids. which is the exact second thing to do. The first thing to do is oxygen. Always remember that.
3
Q
So there is a few things that I want to review, tissue and oxygen perfusion is directly related to mean arterial pressure, and there are three factors that influence mean arterial pressure.
A
The first factor is total employment volume. Second factor is cardiac output, and the third factor is the size of the vascular bed.
4
Q
So if total blood volume and cardiac output are low, mean arterial pressure will be low.
A
If cardiac output and total blood volume are high, the mean arterial pressure will be high.
5
Q
What is the required for minimum mean arterial pressure to perfuse the heart?
A
- So any time that the mean arterial pressure drops below 60, we should start to get nervous.
6
Q
if your heart rate is higher than your systolic pressure…
A
you need to be calling somebody.
7
Q
Now, in terms of the size of the vascular bed, if it becomes larger, the mean arterial pressure drops.
A
So when I say that the vascular bed becomes larger, what am I really saying? Vasodilation. Exactly.
8
Q
So if we had vasoconstriction, and all of a sudden the vascular bed is smaller,…
A
the mean arterial pressure goes up. We get faster flow.
9
Q
What controls vascular bed size ?
A
sympathetic Stimulation. So if you have an increased sympathetic nervous system stimulation, you are going to increase mean arterial pressure.
10
Q
Any issue that impairs oxygen delivery to tissues and organs can start the syndrome of shock.
A
Any issue that impairs oxygen delivery to tissues and organs can start the syndrome of shock.
11
Q
Shock is a syndrome because
A
it occurs in a predictable sequence and pattern.
12
Q
Additionally shock is a metabolic condition, because
A
oxygen delivery is not adequate to meet tissue demand. It represents a whole body response. Everybody’s system is affected by shock.
13
Q
now there are some common cellular changes that occur in all of the types of shock. The first one is…..
A
decreased energy production. So decreased ATP
14
Q
With that decreased energy production comes decreased aerobic metabolism, and increased in aerobic metabolism. What is the outcome of increased anaerobic metabolism?
A
Lactic acid. Which results in what type of acidosis? Metabolic.
15
Q
You have decreased cell function, so whatever the cell is supposed to do, it’s not working right.
A
So if it is a pancreatic cell, you have insulin issues. If it is a heart cell, you have rhythm issues. If it is a lung cell, you may have diffusion issues. So it could be an issue with oxygenation, or what is the other part? Ventilation.
16
Q
You will have altered integrity of the cell membrane. If the cell membrane alters itself, what happens inside the cell?
A
It is going to be “Bad”. The cell is going to explode. We call this process apoptosis. because it is what the cell is doing. It is popping open. With those changes in the cellular environment, you will have an acidosis, electrolyte changes, rupture of the lysosome and then apoptosis.
17
Q
hypovolemic shock. What is really going on here?
A
too little circulating blood volume.What is important here is that in this extracellular fluid, a quarter of this is plasma, and three quarters of this is interstitial.
18
Q
in hypovolemic shock when there is too little circulating blood volume are issue is decreased intravascular volume.. Because of that decreased intravascular volume, we had decreased venous return. What does that sound like?
A
CHF.
19
Q
decreased intravascular volume leads to…
A
decreased venous return…
20
Q
decreased venous return leads to….
A
decreased ventricular filling…
21
Q
decreased ventricular filling…leads to…
A
results in a decreased stroke volume….
22
Q
results in a decreased stroke volume leads to….
A
a decreased cardiac output..
23
Q
a decreased cardiac output leads to…
A
decreased tissue perfusion, which takes us to cellular changes….
24
Q
those cellular changes are those that I just mentioned where you have decreased ATP production,
A
where you have decreased cell function, where you have changes in the cellular environment, and then the cell gets mad and it blows itself up. Suicidal cells.
25
cellular changes are where you have decreased ATP production, where you have decreased cell function, where you have changes in the cellular environment, and then the cell gets mad and it blows itself up. Suicidal cells. So how do we see this in the patient?
Decreased MAP
26
Now what are some causes of hypovolemic shock?
Bleeding, hemorrhage is the number one cause. can be external- Gunshot wounds, stabbings,can be internal- gastric ulcers, varicies, Also causes of hypovolemic shock include-- dehydration from heat exhaustion or vomiting/diarrhea. - elderly- don't drink enough- burns- DKA/DKI with excess UOP
27
If uncorrected, hypovolemic shock will go through 4 predictable stages. The first of those is the early stage…..
where the baseline mean arterial pressure drops by about 10 mmHg. unfortunately we don't tend to see that because the blood pressure usually rises in this phase, as a compensatory mechanism because we have adaptive mechanisms that are working and that is a good thing.***** we had an increased heart rate and respiratory rate, and a slight increase in our diastolic blood pressure. All of this is due to increased vascular tone, from the sympathetic activity. The body is saying “I don't have enough cardiac output, so I'm going to squeeze the vessel a little bit, and I'm going to increase the heart rate. Because I am attempting to affect heart rate times stroke volume equals cardiac output.”
28
Stage 2 Hypovolemic Shock-non-progressive compensatory stage
where the base mean arterial pressure has dropped about 15 mmHg. The adaptive mechanisms are effective for vital organs. So we had good blood flow to the kidney. We have good blood flow to the heart and brain, but the stomach not so much. This is all driven by renal and barrowreceptor response located in the kidney, and hormonal compensation. ****Slight increase in diastolic blood pressure and increase in heart rate and respiratory rate, but you are also going to see an acidosis. Subjectively the patient is going to be anxious. objectively, they are going to be restless, they are going to have tachycardia, tachypnea, a decreasing urinary output, their systolic blood pressure will be dropping, diastolic blood pressure will be rising.They will have cool extremities, and you will begin to notice a 2 to 5% decrease in their stats. Their oxygen saturation’s… so if they were at 100%, they are now at 95%. If they were at 90%, they are now at about 86%.
29
In the progressive stage, or stage three hypovolemic shock...
the mean arterial pressure has now dropped about 20 mmHg. The adaptive mechanisms are less effective but still functional that there is not enough oxygen to the vital organs. So we had poor oxygenation. Because of this, we have a buildup of toxic metabolites, and cellular death. So the vital organs are hypoxic, and the non-vital organs are anoxic. The vital organs are hypoxic, so there is some oxygen there but not enough, the nonvital organs are a anoxic, there is no oxygen there. Skin, G.I. tract. Subjectively is severe thirst, deeper anxiety with impending doom. I am going to die. Objectively, they will have a rapid but weak pulse, a low blood pressure… We are now systolic less than 90, possibly even less than 80…, They will be pale to cyanotic, cool and moist skin and anuric. you will now notice up to a 20% drop in their sats. So if they were at 100% they are now at 80%. They will have a low blood pH. They will have an increased lactic acid level and an increased potassium. When you see these symptoms, you have about one hour to save this patient's life, or we will end up in the refractory or irreversible stage.
30
Stage 4 refractory or irreversible stage Hypovolemic Shock...
At this point, it doesn't matter what you do there has been too much tissue damage. Even if the shock is corrected and the mean arterial pressure returns to normal, there is too much cellular damage for the organism to survive. Signs and symptoms of the refractory stage is a rapid loss of consciousness, non palpable pulse, , cold and dusky extremities… Like the patient will look grey, slow and shallow respirations, almost like guppy breathing. Their sats will be not measurable anymore. You will not be able to pick up a waveform. Once we have widespread release of toxins, they will develop what is called mods. Multiple organ dysfunction syndrome. And once it starts it is a cycle. And it just gets worse, and we can't reverse it.
31
Here is what you should always remember, for every body system that you lose, mortality increases by 10%
So if you have lost your liver function, your heart function, kidneys, now your moms, now your pancreas is gone…. That right there is a 50% mortality rate. So if I go in and have some condition that already has my mortality rate at 80% or 20% and I start losing organ function on top of that it starts to multiply. So as you are watching patients, remember that the skin is also considered a organ system, they can have decubitus ulcers, if they are intubated, those are two systems that are not functioning on their own. If they have some type of inotrope or vasopressor being used, that is three systems that we are controlling. If they are also on bedside dialysis, thats 4. If they are being fed with the NG tube thats 4 or TPN or liquids we are now up to five. So my mortality rate is up to 70 or 80%. Those patients require constant supervision by you the nurse.
32
So what are we doing to prevent Hypovolemic Shock?
Well, we are going to teach patients about adequate fluid intake during exercise and hot and dry environments. Because you can lose a large amount of fluid without having knowledge of it. We are going to use proper safety equipment and seatbelts to prevent trauma and hemorrhaging. And we're going to be aware of hazards in the home or workplace.
33
Risk Factors For Hypovolemic Shock..
Being in the HospitalSo ID those at risk for dehydration, you can find these things on pages 175-176 but specifically I am speaking about ****reduced cognition, reduced mobility, and in order to be NPO. So if I can't move and I can't tell you that I'm thirsty and you are not letting me drink anything…. You need to be thinking that I have a risk for hypovolemia.
34
Assessments for Hypovolemic Shock...
Assess post invasive procedures for obvious and occult bleeding, compare pulse quality and effectiveness with the baseline. Compare urinary output to fluid intake. Check the vital signs if the patient complains of a severe thirst. ***If in the outpatient setting, watch for obvious heavy bleeding, persistent thirst, decreased urinary output, lightheadedness, and a sense of impending doom. Why are they lightheaded? Not enough oxygen, because there isn't enough fluid to get up there, so those things that I have just said, I want you to keep in mind, is that you can lose a large amount of fluid without knowing it. Especially in hot dry environments. ****And in the outpatient setting, you really need to teach patients to let you know if they have a decreased urinary output or if they get lightheaded and dizzy when they standup.
35
Class I Hypovolemic Shock
they have lost about 15% of their bodily fluid, less than a liter. Not much we're going to do about that, the body will probably take care of itself. Might give them some PO fluids.
36
Class 2 Hypovolemic Shock
they have lost about 15 to 30% so we are going to give them IV fluids. Lactated ringers is what our choice is. But before you get the fluids, our priority intervention is oxygen. Then we will get to the fluids. So one exam I may say to you that the patient has oxygen on, what is your next priority. What will the next priority be? Fluids…. Not setting them upright in the bed. this is not an issue of ventilation, this is an issue of oxygenation. And they have to have fluids to move the oxygen through.
37
Class 3 Hypovolemic Shock
we are not only going to be giving IV fluids, because the patient has lost about 2 L, we are going to start getting some blood products as well. If I give too many IV fluids and not enough blood to go with it, then I hyper dilute the patient. So essentially artificially dropping their hematocrit.
38
Class 4 Hypovolemic Shock
we are going to have to move beyond fluids and blood, and we are going to have to use volume expanders and vasoactive drips which we will come to more detail about those later. But… Specifically I want you to know dopamine. And what is dopamine really supposed to do? Increases cardiac output. ****oxygen, ringers lactate which is a crystalloid , and dopamine…
39
cardiogenic shockPathophysiologically, you have myocardial insult. ….
And with that you have loss of critical mass. Well, what does that mean? That means the ventricle is broke and it don't work no more. Then from that you have impaired ventricular function and from there we are here… Where you have decreased stroke volume, decreased cardiac output, decreased tissue perfusion, cellular changes. But if you have decreased cardiac output and decreased blood pressure what goes along with that for the heart? Decreased perfusion pressure. So you have decreased coronary perfusion. You end up with myocardial ischemia and necrosis, so you have an unhealthy heart muscle that has an impaired pump action and really what is going on here with this impaired off action is reduced systolic emptying. So when I pump I don't get as good as squeeze and I don't get as good as output as I want. I don't get as good of squeeze, I don't get as good of output.
40
The most common cause of cardiogenic shock is…..
heart failure from MI. We call that coronary cardiogenic shock. It is associated with coronary artery disease, and as a result in MI and cumulative necrosis of 40% or more of the left ventricle.
41
The other causes that you see there, non-coronary cardiogenic shock is related to…..
1. dysrhythmias, 2. end stage cardiomyopathy's, 3. congestive heart failure, 4. heart valve abnormalities, 5. pericardial tamponade. The essence for non-coronary cardiogenic shock is that it is occurring in the absence of coronary artery disease. And the related conditions are the ones I just described.
42
So what really is cardiogenic shock then?
It is shock that is characterized by a decrease in cardiac output related to impaired heart function.That is all cardiogenic shock is. If the heart tissue is necrotic it doesn't squeeze and when I get to about 40% damage that's when I end up in this cardiogenic shock state. And, it is the coronary cardiogenic shock…
43
distributive shock….
Is volume loss that is internal or it has to do with redistribution of the interstitial tissue. These are the patients who are described in shock as warm and pink, because they have vasodilated out.Of these, neural induced, we call that neurogenic shock. So for neurogenic, think about disorders of the brain and spine. So if you were to have a closed head injury. That could result in a neurogenic distributive style shock because the patient will become bradycardia, they will lose sympathetic tone, so they dilate out. And when they dilate out, there is not enough fluid left in the vessel so the pressure drops. When the pressure drops, you end up with decreased venous return, you end up with decreased ventricular filling, you end up with decreased stroke volume, you end up with decreased cardiac output, which results in decreased tissue perfusion, and cellular changes that result in apoptosis.... it's all the same. It's just what is causing it that is different.
44
Some other things that can cause neurogenic style shock?
****Closed Head Injuries if high levels of spinal anesthesia/Epidural, Severe Paininsulin shock
45
chemical induced Shock
anaphylaxis, sepsis, and capillary leak syndrome.
46
anaphylaxis
That is antigen antibody issues…. Release of histamine and other vasoactive chemicals.
47
What is our number one symptom for a anaphylactic reaction?
swelling caused by edemaSo what would you ask the patient when you walk in and see them? are you always this puffy?
48
So what is really going on with anaphylaxis?
it is an immediate hypersensitivity reaction where we have IGE antibody and mast cells and circulating basophils. And what is really happening there is a decreased cardiac output. We are back here again....to decreased cardiac output, decreased tissue perfusion, cellular changes.
49
And with capillary leak syndrome you can see that in…..
burns, liver disorders, acites, peritonitis, paralytic ileus, severe malnutrition, where are these issues? In the G.I. tract and the gut. you can see it with large wounds, hyperglycemia, kidney disease, Hyperprotienemia and trauma.
50
So if we have some kind of abdominal issue going on, capillary leak syndrome is something that you need to be thinking about.
Of all of those things that i have just listed off, the 2 that are the most important are burns and decreased serum protein So capillary leak syndrome is just an issue of blood vessel integrity loss due to protein changes.
51
Obstructive shock
it is any time the heart muscle is prevented from pumping effectively.Pericarditis, tamponade, pneumothorax, embolus, and aortic stenosis. So any issue that prevents the heart from ejecting blood is an obstructive style of shock.
52
SEPSIS- there is a host of related factors and treatment related factors that go with it... and sometimes we cause sepsis in these patients….
This is caused by nosocomial infectionsWhat are iatrogenic?Don’t know the cause..or it came from outside the hospital setting.
53
Related factors for sepsis are
age, genetics, chronic health problems, malnutrition, debilitation, pregnancy, ****splenectomy,
54
Splenectomy
Because many many many trauma patients end up with a splenectomy. Especially if there is left sided injury..they will go ahead and take the spleen out so that the patient doesn’t bleed to death. So if we take the spleen out it increases the patients risk for sepsis.
55
treatment related factors that cause sepsis
hospital environment, instrumentation, surgical procedures, wounds, invasive diagnostics, traumatic wounds, thermal injuries, ****immunosuppression***widespread use of antibiotics.
56
And all of sepsis is related to the white blood cell system.
so you have interleukins, and tumor necrosis factors and complement fragments and all kinds of stuff going on
57
So keep in mind that the causes and the initial manifestations of shock
may vary...eventually the effects of hypotension and anaerobic cellular metabolism result in common key features.
58
Within the cardiovascular system..
Decreased cardiac output, increased heart rate with decreased quality...so yes it is faster but when I feel it...it’s weaker….decreased systolic pressure, narrowed pulse pressure…You’ll notice postural hypotension...So if the patient has postural hypotension..They will have flat neck and hand veins...even in dependent positions….Make sure that you have good big IV’s to start with....cause once you get to this point....it’s gonna be really hard to stick the patient... They will have a slow capillary refill and diminished peripheral pulses.
59
what is a narrowed pulse pressure?
Systolic and diastolic are coming together..
60
What test can you conduct...to see that?
Orthostatics.
61
In the pulmonary system...
tachypnea...shallow respirations...increased co2 decreased 02….and they will be cyanotic from the lips and the nail beds.
62
Alright increased co2..what do you think?
respiratory acidosis.
63
Decreased Pa02 What do we call that?
hypoxemia.
64
Key features in the neuro system
notice that I have early and late signs. Please try to recognize these early. Anxiety and restlessness and increased thirst. You need to be doing something AT THAT point. Not waiting for them to become comatose with sluggish pupils. I have told you before First thing a neuro nurse will do when they walk into a code is check the patients pupils. If they are fixed and dilated we stop CPR. There is no reason to continue when the brain is already dead....
65
Early Neuro Signs
Anxiety and restlessness and increased thirst.
66
Late Neuro Signs
comatose with sluggish pupils.
67
Renally..
Decreased urine output. Increased specific gravity. Why does specific gravity go up? Because the urine is concentrated.
68
In the integumentary system.
They are cool to cold. Unless they are??? Not. If they are warm, what type of shock is that. distributive. They will be pale to mottled to cyanotic.Early in the mucus membranes...late more dependent. These are the patients that when you look at them laying in the bed., in the late phases...They look like they have a purple robe going across their lower back.So from mid-axillary line backwards. They will look mottled. Little purple roadways all across the skin.. And they may be moist and clammy.
69
Are these the patients that you need to be changing the sheets on?
NO! If you start flipping these people around they are already orthostatic..HERE lets just keep changing their pressures and they just get worse and worse and worse.
70
Laboratory wise..
they will have a decreased hematocrit and hemoglobin...if they have hemorrhaging. If they have dehydration or fluid shifts...they will have an increased hematocrit and hemoglobin. On the ABG what you will likely see is a mixed acidosis. Respiratory and metabolic
71
So you have 4 priority problems..for patients with shock
1. hypoxia related to hypovolemia.2. hypoperfusion related to active fluid volume loss and hypotension. 3. anxiety...yours and the patients...related to potential for death...and decreased cerebral perfusion4. confusion...related to decreased cerebral perfusion.
72
hypoxia related to hypovolemia. treatment?
oxygen
73
hypoperfusion related to active fluid volume loss and hypotension treatment?
fluids. Which fluids? Lactated ringers... you can give normal saline but lactated ringers is usually the choice. You may also see that answer as...crystalloids.
74
So when you think about interventions...there are three things to consider.
1. you must reverse the shock.2. you must restore fluid volume.3. you must prevent complications.. Monitoring.among these monitoring is critical.
75
What will you be monitoring to prevent complications...
vital signs and level of consciousness
76
Non-surgical Interventions-
oxygen therapy to reduce damage from tissue hypoxia.IV therapy of fluid resuscitation use LR.. crystalloidscolloids- that is packed red blood cells, whole blood, plasma, synthetic plasma, expanders like hespan..albumin...and dextran 40..So you may do vasoactive agents. vasoconstrictors like dopamine and norepinephrine...and inotropes like dobutamine and milirinone. You should be monitoring pulse pressure…and mean arterial pressure…skin and mucosal color....UOP and LOC….and vital signs..every 30 to 60 min.......
77
Hesban-
has ANTI- Platelet effectsmakes you bleed
78
Dextran 40-
makes you clot
79
Albumin-
makes you swollen
80
When do we give vasoactives?
When volume replacement is not sufficient to restore blood pressure...if I cannot pump enough volume into you to expand your blood pressure then I need to do something to the pipe and I am going to squeeze it down....or I am going to do something to the pump to make it pump more effectively.....
81
So Sepsis and septic shock is a complex type of distributive shock beginning as a bacterial or fungal infection...Who gets this?
Who is more likely to get this among hospitalized patients….Diabetes..drug users.. the immunosuppressed...HIV.. What you end up with is a systemic infection...
82
Please know that local infections do not cause sepsis...
So if you get a little cut on your finger..you are not going to become septic..unless that infection becomes systemic...Then we have a whole new issue....
83
So systemic infections we call early sepsis....
That is going to move to something called SIRS...S-I-R-S...Systemic Inflammatory Response Syndrome..Then we are going to end up in severe sepsis what we call organ failure.and then from there MODS...Multiple organ dysfunction syndrome....and from there,,, Death... Unless we break the cycle...
84
Which kind of infections lead to systemic infections?
UTI’s BSI’s and BAP’s CAUTI CLABSI and VAP. Central line associated blood stream infections....CLABSI…Catheter associated Urinary tract infections CAUTI….and VAP Ventilator associated Pneumonias...
85
So these are the key features of SIRS...
Temperature will be less than 96.8. or greater than 100.4. The heart rate will be greater than 90. The respiratory rate will be greater than 20....and look at the WBC’s ….the patient will have a low grade fever...mild tachycardia,,.,,and hypotension with a lower than expected urinary output..Now you see at the very bottom under WBC’s that I have 10% bands..Band cells should be between 3 and 5%. anything greater than 7% is a sign of severe inflammation....Because the band cells are neutrophils that are undergoing granulopoiesis...that means that they’re just growing..from metamyelocytes to mature granulocytes...doesn’t matter about all of those big words....band cells are neutrophils that are aging...and you want them somewhere between 3 and 5%. anything greater than 7% is indicative of severe inflammation….Is there anything that you can think of that would perhaps raise your band cell count that is not related to SIRS? Arthritis....and Leukemia...so any of the white cell cancers and any of the joint disorders...
86
Band cells should be between 3 and 5%. anything greater than 7% is a sign of
Severe inflammation
87
We start out with cell anoxia and organ failure, that causes more cell anoxia and cell death in the vital organs..
then we become more hypo-dynamic..and then we end up with more cell hypoxia....and then we end up with more cell anoxia....as we do that we end up with SIRS, Organ Failure, Multiple Organ Dysfunction, Syndrome, Prolonged organ failure, irreversible damage, organism death, That is what is going on with all of this SIRS stuff..
88
If we recognize this issue early.. good outcomes are possible...IF we don’t it will progress quickly and the patient will likely die...So what are we really looking for?
Cell hypoxia and reduced organ function…There is an increased number of cells opporating under anaerobic metabolism so what blood marker are you going to want to monitor? Latate…There will be more toxins and more pro-inflammatory cytokines which all just goes to amplify this effect of SIRS...
89
Wide spread Micro-thrombi resulting in DIC. Disseminated Intravascular Coagulation.
***..You will know this because their IV’s will start to bleed.The reason that we have this wide-spread micro thrombi issue and the reason why the patient is bleeding out is because it consumes all of the available platelets and clotting factors…***So initially....We will give heparin to prevent micro thrombi formation….or Dextran 40
90
If they have DIC the other thing they may notice is petechia and ecchymosis. and keep in mind we now have thousands of small clots floating around the body so they are going to be in the liver, the kidney, the brain, the spleen, the heart..
.so if they are in the lungs than you can see that similar to ARDS…decreased SATS, they will be hypoxic, and they will be ischemic…They will have a prolonged aPTT and they will have an elevated D-Dimer…If you ever see the test D-Dimer ordered, the Physician or the nurse practitioner is thinking the patient is in DIC. That is the only thing that test is used for….And if the lab tells you that it is high...they probably got DIC…So then you are going to watch for are they bleeding...If they are not bleeding you are likely going to give some kind of anticoagulant...but once they start bleeding...then we turn the anticoagulants off...
91
So we talked about risks...Table 39-4 gives you some additional risks beyond immunosuppression
.and one of those is malnutrition from hepatitis in alcoholics..The other is large open wounds and the last one is patients greater than 80 years of age….All of those patients are at risk for sepsis..
92
So really what we can do is try to prevent it using aseptic technique,
remove IV’s and urinary catheters as soon as we possibly can…Assess vital signs often..You are going to review labs but keep in mind that single blood test will confirm the presence of sepsis or septic shock..prevention is the best management strategy.If the patients are older than 65 they have 2 times the risk of mortality..So if they normally had a 20% mortality from sepsis they now have a 40% mortality if they are over the age of 65.blood cultures is that they should be done as soon as possible.
93
The priority problem for patients with septic shock is
the potential for multiple organ dysfunction syndrome….and what you are looking for is normal aerobic cellular metabolism....So the ABG should be normal....Urine output of at least 30ml. Mean arterial pressure within about 10mm/hg of baseline. and absence of multi-organ dysfunction syndrome..So stable pressure...Stable labs...Decent urine output.....That is what you want..
94
It is the severe sepsis 3 hour recusitation bundle
where you measure the serum lactate and you draw your blood cultures prior to the antibiotics.The new recommendations for crystalloids or colloids is now 30ml/kg not 20....So we are going to give more volume than we used to give..... and we are going to do that for any for any hypotension or any lactate level that is greater than 4mmol/L.
95
6 hour septic shock bundle
.So for unresolved hypotension after a fluid bolus...mean arterial pressure is still less than 65 we are going to add vasopressors..Norepinephrine or Neosynephrine.we are going to give low dose steroids....because of an issue of adrenal insufficiency....that is due to a stress response....What does the adrenal gland secrete? that we care about? cortisol is one and aldosterone is the other....aldosterone is the water and sodium.....saving hormone.....and once the adrenal gland has been required to secrete and secrete and secrete and secrete and secrete that kind of runs out...runs low so it becomes insufficient...to maintain blood pressure.....and with adrenal insufficiency we have an increased risk of hyperkalemia....and we have an increased risk for infection...all of this is now part of the 6 hour bundle.
96
Now what antibiotics are they going to use?
Ancef. So the cefazolins and the aminoglycosides. Put a circle around Ancef...
97
Blood replacement therapy for late stage septic shock where we are going to give clotting factors like.
.cryoprecipitate, FFP, Whole blood, and packed red blood cells...
98
.Now if we are going to send these patients home after they have recovered from septic shock there are some things we are going to want them to do..
.one of those..we are going to want them to clean their toothbrush daily....by running it through the dishwasher or pouring clorox over it…..We want them to bathe daily with antimicrobial soap...specifically their armpits, their groin, and the rectum….and we never want them to clean a pet litter box again....So it is almost worth getting sepsis if you have a cat
99
Which clinical manifestations would you expect to assess in the compensatory stage of hypovolemic shock...
increased heart rate slight tachycardia, increased blood pressure slight hypertension...specifically diastolic and because of that.narrowed pulse pressure….decreased urine output slightly....and what about the gut? decreased motility that results in decreased bowel sounds....
100
Septic shock is a serious and life threatening condition, what type of patients are at risk for sepsis?
diabetes, immunosuppressed, elderly.
101
What is the priority intervention for patients with septic shock?
Blood cultures.....they will likely already have the oxygen on...Then give any prescribed antibiotics....And why do we give anticoagulants to patients with septic shock....to counteract DIC and control their bleeding issues....fabulous.....That is the end of the lecture...
