shock states - cdn.ymaws.com
TRANSCRIPT
![Page 1: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/1.jpg)
Lynn Fitzgerald Macksey
RN, MSN, CRNA
SHOCK STATES
![Page 2: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/2.jpg)
Define SHOCK
: a state where tissue perfusion
to vital organs is inadequate.
![Page 3: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/3.jpg)
Shock state
In all shock states,
the ultimate result is inadequate tissue
perfusion, leading to a decreased
delivery of oxygen and nutrients to
cells….
and, therefore, cell energy.
![Page 4: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/4.jpg)
Clinical recognition of shock
Symptoms
dizziness, nausea, visual changes, thirst,
dyspnea
Signs
cold clammy skin, pallor, confusion,
agitation, diaphoresis, weak thready
pulse, obvious injury
![Page 5: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/5.jpg)
Compensatory stages of shock
Sympathetic nervous system
Renin-angiotensin system
Pituitary-antidiuretic hormone release
Shunting from less critical areas to brain
and heart
![Page 6: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/6.jpg)
Progressive decompensation
Failure of compensatory mechanisms in
Bowel
CNS & autonomic
Heart
Kidneys
Lungs
Liver
What will we see?
![Page 7: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/7.jpg)
Shock diagnosis
Clinical examination
Diagnostics:
CXR
CBC
blood chemistry
EKG
ABG
vital signs
![Page 8: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/8.jpg)
Monitoring organ perfusion
in shock states
Base deficit
Blood lactate levels
Normalization of these markers are the end point
goals of resuscitation!
![Page 9: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/9.jpg)
Base Deficit
Reflects severity of shock, the oxygen
debt, changes in oxygen delivery, and
the adequacy of fluid resuscitation.
2-5 mmol/L suggests mild shock
6-14 mmol/L indicates moderate shock
> 14 mmol/L is a sign of severe shock
![Page 10: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/10.jpg)
Base Deficit
The base deficit reflects the likelihood of
multiple organ failure and survival.
An admission base deficit in excess of 5-8
mmol/L correlates with increased mortality.
![Page 11: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/11.jpg)
Lactate Levels
Blood lactate levels correlate with other
signs of hypoperfusion.
Normal lactate levels are
0.5-1.5 mmol/L
>5 mmol/L indicate significant lactic
acidosis.
![Page 12: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/12.jpg)
Lactate Levels
Failure to clear lactate within 24 hours
after circulatory shock is a predictor of
increased mortality.
![Page 13: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/13.jpg)
Types of shock
Hemorrhagic/hypovolemic
Cardiogenic
Neurogenic
Septic
Anaphylactic
![Page 14: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/14.jpg)
HEMORRHAGIC /
HYPOVOLEMIC SHOCK
Loss of intravascular volume –
![Page 15: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/15.jpg)
HEMORRHAGIC/HYPOVOLEMIC SHOCK
Causes:
Hemorrhage
Low filling pressures lead to decreased
cardiac output
Low hemoglobin levels lead to a
reduction in tissue oxygen delivery
![Page 16: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/16.jpg)
HEMORRHAGIC/HYPOVOLEMIC SHOCK
Causes:
Hypovolemia
Severe dehydration
Secondary to fluid redistribution
i.e. burns, surgery (3rd spacing)
![Page 17: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/17.jpg)
Symptoms of hypovolemic shock
Anxiety, irritability, decreased level of
consciousness, tachycardia,
hypotension, tachypnea.
Hemodynamics:
Decreased CVP, PAP, PCWP, CO
Increased SVR
![Page 18: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/18.jpg)
HEMORRHAGIC/HYPOVOLEMIC SHOCK
Any major volume loss causes
compensatory mechanisms to kick-in to
maintain BP and tissue perfusion.
These include…..
![Page 19: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/19.jpg)
HEMORRHAGIC/HYPOVOLEMIC SHOCK
Vasoconstrictor Response: sympathetic nervous system triggers
adrenal medulla to secrete –
**epinephrine and
**norepinephrine
increasing peripheral vascular resistance and
reducing size of vascular department.
![Page 20: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/20.jpg)
HEMORRHAGIC/HYPOVOLEMIC SHOCK
Kidneys: decreased blood flow through kidney causes decreased glomerular filtration = decreased urine.
When blood pressure decreases, kidney produces renin.
![Page 21: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/21.jpg)
HEMORRHAGIC/HYPOVOLEMIC SHOCK
Low BP?
Kidney secretes Renin
Renin cleaves angiotensinogen angiotensin I
= angiotensin II
Angiotensin II –vasoconstrictor
![Page 22: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/22.jpg)
HEMORRHAGIC/HYPOVOLEMIC SHOCK
Angiotensin II stimulates adrenal cortex to produce aldosterone: conserves water and sodium and decreases secretion of water.
Decreased blood volume also stimulates hypothalamus, which regulates ADH (antidiuretic hormone/Vasopressin) decreasing amount of urinary output.
![Page 23: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/23.jpg)
HEMORRHAGIC/HYPOVOLEMIC SHOCK
Early and appropriate resuscitation may
avert damage to individual organs as
adaptive mechanisms act to preserve the
organism.
![Page 24: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/24.jpg)
HEMORRHAGIC/HYPOVOLEMIC SHOCK
1st and foremost…
Identify underlying cause of bleeding or hypovolemia and stop it.
Hold pressure over source of external bleeding.
Head down position to move blood out of legs and into thorax and head
![Page 25: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/25.jpg)
HEMORRHAGIC/HYPOVOLEMIC SHOCK
FILL ‘ER UP!
“Heart rate, systemic blood pressure, pulse
pressure, respiratory rate, urine output, and
mental status remain the best available early
clinical indicators of the severity of
hemorrhagic shock.”
![Page 26: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/26.jpg)
HEMORRHAGIC/HYPOVOLEMIC SHOCK
The response of the pulse and blood pressure to initial fluid therapy also aids in the assessment of hypovolemia.
Giving LR 2,000 ml over 15 minutes in adults, or 20 ml/kg in children, should normalize vital signs if hemorrhage is mild (10-20%)
![Page 27: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/27.jpg)
HEMORRHAGIC/HYPOVOLEMIC SHOCK
A transient improvement after fluid infusion suggests a 20-40% decrease in circulating volume or continuing blood loss – more crystalloids and possibly blood transfusion are required in these patients.
![Page 28: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/28.jpg)
HEMORRHAGIC/HYPOVOLEMIC SHOCK
If the VS do NOT respond to this initial fluid resuscitation, there has probably been severe (>40%) blood loss – replace by rapid infusion of crystalloids, colloids, and blood.
We also draw labs and transfuse based on the H&H levels.
![Page 29: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/29.jpg)
Fluid resuscitation
Rapid
response
Transient
response
Minimal or
No
response
Vital Signs Return to normal Transient
improvement
Remain
abnormal
Estimated blood loss Minimal
10-20%
Moderate, ongoing
20-40%
Severe
>40%
Need for crystalloid Low High High
Need for blood Low Moderate to high Immediate
Blood preparation Type & cross Type specific Not type-
specific
Need for surgery Possible Likely Highly likely
Early surgeon presence Yes Yes Yes
Barash
![Page 30: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/30.jpg)
Massive transfusion guideline
PRBCS Plasma Platelets Cryoprecipitate
6 units 6 units
6 units 6 units 1 apheresis
6 units 6 units 10 units
6 units 6 units 1 apheresis
6 units 6 units 10 units
6 units 6 units 1 apheresis
6 units 6 units 10 units
Grady Memorial Massive Transfusion protocols
![Page 31: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/31.jpg)
CARDIOGENIC SHOCK
pump failure, or
obstruction of cardiac filling
increased venous return
very decreased cardiac output
increased afterload (SVR)
![Page 32: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/32.jpg)
CARDIOGENIC SHOCK
Pump failure:
myocardial infarction
dysrhythmias
ventricular septal defect
cardiomyopathies
valve disorders
pulmonary hypertension
![Page 33: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/33.jpg)
CARDIOGENIC SHOCK
Hallmark signs in cardiogenic shock characterized by:
decreased urine output
altered mentation
hypotension
![Page 34: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/34.jpg)
CARDIOGENIC SHOCK
Hemodynamics:
Increased: CVP, PCWP, SVR
Decreased: CO
![Page 35: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/35.jpg)
CARDIOGENIC SHOCK
Early signs and symptoms are due to strong sympathetic stimulation:
dilates brain vessels and coronary arteries
clamps all other arteries
increased heart rate and blood pressure
BUT
Perfusion pressure low (confused, clammy, decreased urinary output).
![Page 36: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/36.jpg)
CARDIOGENIC SHOCK
Late changes in cardiogenic shock
due to:
MDF (myocardial depressive factor)
blood pooling
platelet aggregation
released toxins
anaerobic metabolism and lactic acidosis
![Page 37: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/37.jpg)
CARDIOGENIC SHOCK
Late signs and symptoms:
Tachycardia and arrhythmias
Absent/decreased peripheral pulses
Cool and clammy skin
Gallop S3 and S4
Pulmonary crackles and edema
Distended jugular veins
![Page 38: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/38.jpg)
CARDIOGENIC SHOCK
Treatment:
inotropes – increased contractility and decreases SVR (afterload). i.e.: dobutamine
Milrinone – phosphodiesterase inhibitor: increases cAMP and calcium
Diuretics – decrease preload and afterload i.e.: furosemide
![Page 39: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/39.jpg)
CARDIOGENIC SHOCK
Oxygen
Decrease myocardial oxygen demand
Intra-aortic balloon pump
antiarrhythmics
![Page 40: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/40.jpg)
CARDIOGENIC SHOCK
Obstruction of cardiac filling:
cardiac tamponade
tension pneumothorax
massive pulmonary embolism
![Page 41: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/41.jpg)
CARDIOGENIC SHOCK
Hemodynamics
Increased CVP
Decreased CO
Treatment of obstructive cardiogenic
shock
Get rid of the obstruction
![Page 42: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/42.jpg)
NEUROGENIC SHOCK
Caused by the sudden loss of the autonomic nervous system signals to the smooth muscle in vessel walls.
![Page 43: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/43.jpg)
Loss of background sympathetic stimulation. Blood vessels suddenly relax resulting in a sudden decrease in peripheral vascular resistance and hypotension.
decreased preload, CVP
very decreased afterload
decreased cardiac output
![Page 44: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/44.jpg)
NEUROGENIC SHOCK
This can result from severe damage to
the
Brain (CNS)
Spinal cord
spinal anesthesia
spinal cord injury
![Page 45: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/45.jpg)
NEUROGENIC SHOCK
S/S of neurogenic shock:
Profound hypotension
Bradycardia
Restlessness, confusion
Warm, dry extremities – no sweating
Peripheral vasodilation
Venous pooling
oliguria
![Page 46: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/46.jpg)
NEUROGENIC SHOCK
Treatment: Support hemodynamics until neurologic
status stabilized
Large volumes of fluid may be needed to
restore normal hemodynamics
Dopamine
Vasopressors i.e. epinephrine
Atropine
![Page 47: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/47.jpg)
SEPSIS - SEPTIC SHOCK
Series of events triggered not only by an invading microbe, but also to a larger extent by the substances released from the microbes
and
the body’s defense against this invasion.
![Page 48: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/48.jpg)
SEPSIS - SEPTIC SHOCK
SIRS – Systemic Inflammatory
Response
At least three of the following criteria must
be present –
Tachycardia (HR > 90 bpm)
Tachypnea (or requirement of mechanical vent)
Hyper- or hypothermia (< 36 or > 38 degrees C)
WBC < 4,000 or > 12,000
![Page 49: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/49.jpg)
SEPSIS - SEPTIC SHOCK
#1 cause is gram-negative bacteria (Klebsiella, pseudomonas, E.Coli, proteus).
Can also be from gram + cocci.
34% from urinary tract infection.
** Overwhelming occurrence from
overwhelming infection **
![Page 50: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/50.jpg)
SEPSIS - SEPTIC SHOCK
Gram-negative infection releases endotoxins. An endotoxin in the blood causes some cells to release histamine -a powerful vasodilator- this dilates all blood vessels especially capillaries.
![Page 51: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/51.jpg)
SEPSIS - SEPTIC SHOCK
You have the right amount of blood but vessels are so dilated the blood is pooled.
Microbes or endotoxins trigger the release of: endorphins
prostaglandins
vasoactive substances: histamine and bradykinin.
![Page 52: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/52.jpg)
First stage of SEPTIC SHOCK
Warm Stage / Hyperdynamic
Stage
3 minutes to 12-16 hours long.
(Almost never picked up)
![Page 53: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/53.jpg)
S/S of 1ST stage of SEPTIC SHOCK
S/S of warm stage of septic shock
normal temperature
great cardiac output 9-11 liters/minute
(endotoxins work on myocardium to increase heart contractility 50%
pulse bounding, good blood pressure
hyperventilation: endotoxins work on the medulla oblongata to increase respiratory rate (not panting but subtle: respiration rate increases to 26-30)
![Page 54: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/54.jpg)
S/S of 1ST stage of SEPTIC SHOCK
ABG’s are excellent (because respiratory rate is increased)
kidneys: vessels vasodilate; Bowman’s capsule filtering increased amounts of blood; patient’s have a great urine output.
confused, though, because endotoxins work on brain.
![Page 55: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/55.jpg)
Treatment of 1st stage of SEPTIC SHOCK
Treatment must be done in WARM STAGE
FLUID AND ANTIBIOTICS!!!!!
Give 200cc IV fluid per hour so when patient goes into cold stage, body won’t suffer from low BP
Give Dopamine: vasoconstricts capillaries so they can’t pool blood
Find infection and get rid of it.
![Page 56: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/56.jpg)
Second stage of SEPTIC SHOCK
COLD STAGE
All blood vessels vasodilate and
pools/stagnates in capillaries.
Pre-capillary sphincter relaxes but not post-
capillary – the blood dumps in but not out.
![Page 57: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/57.jpg)
S/S of 2nd stage of SEPTIC SHOCK
S/S:
hypotension
decreased pulse
cold, mottled skin
no urinary output
ischemia, arrhythmias, acidosis,
decreased stroke volume and cardiac
output.
![Page 58: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/58.jpg)
When compensatory mechanisms fail…
Mortality rate in septic shock is 80-90%.
![Page 59: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/59.jpg)
ANAPHYLACTIC SHOCK
Allergic response triggers mast
cells to release immunological
mediators (i.e.: histamine,
prostaglandins, leukotrienes, etc.)
causing:
systemic vasodilation
edema of bronchial mucosa,
bronchoconstriction, and dyspnea
angioedema
![Page 60: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/60.jpg)
ANAPHYLACTIC SHOCK
Anaphylactic shock can lead to
death in a matter of minutes if
left untreated.
![Page 61: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/61.jpg)
ANAPHYLACTIC SHOCK
Common causes of anaphylactic shock:
Food: Peanuts, walnuts, cashews, shellfish, fish, milk, and eggs
Medications: NSAIDS, IV contrast, blood products
Anesthetics: NDMR, latex, antibiotics, colloids, induction agents, and local anesthetics
Insect stings: bees, wasps, hornets
![Page 62: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/62.jpg)
ANAPHYLACTIC SHOCK
S/S:
respiratory distress
hypotension
urticaria
flushed appearance
angioedema: swelling of lips, face, neck, and throat
Anxiety
Tachycardia, hypotension
![Page 63: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/63.jpg)
ANAPHYLACTIC SHOCK
Hemodynamics
Decreased CVP
Decreased PCWP
Decreased SVR
![Page 64: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/64.jpg)
ANAPHYLACTIC SHOCK
Treatment:
Stop administration or decrease absorption of offending agent if possible.
Give:
Epinephrine
Antihistamines H1 and H2 blockers
Racemic Epinephrine for laryngeal edema or laryngospasm
Airway control: endotracheal intubation or tracheostomy
Hydrocortisone 100-150 mg IV q 6 hrs. - stabilize cell membrane for persistent symptoms
Fluid resuscitation
![Page 65: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/65.jpg)
FAILURE OF COMPENSATORY
MECHANISMS in SHOCK
Myocardial: ultimately results in:
increased myocardial ischemia
decreased contractility (acidosis, myocardial depressive factor)
increased dysrhythmias
![Page 66: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/66.jpg)
FAILURE OF COMPENSATORY
MECHANISMS in SHOCK
Cerebral ischemia:
initially results in stimulation of the SNS, if prolonged there will be a loss of sympathetic influences.
![Page 67: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/67.jpg)
FAILURE OF COMPENSATORY
MECHANISMS in SHOCK
Kidney
Decreased blood pressure → kidney tubules necrotic → acute tubular necrosis (ATN)
![Page 68: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/68.jpg)
FAILURE OF COMPENSATORY
MECHANISMS in SHOCK
Microcirculation:
Thrombosis of small vessels secondary to:
Blood stagnating within the capillary bed
Acidosis and catecholamines increases platelet aggregation
Damage to endothelial lining of cells
![Page 69: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/69.jpg)
FAILURE OF COMPENSATORY
MECHANISMS in SHOCK
Acidosis: worsened by:
Increased production of lactic acids with poor tissue perfusion
Decreased renal function
Decreased respiratory function, hypoxia, and hypercapnia (more acids)
![Page 70: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/70.jpg)
Complications of shock
HYPOTENSION (cardiac output low)
LUNGS KIDNEYS PANCREAS kills Type 2 alveolar cells kidney tubules pancreas releases MDF
no surfactant ARDS necrotic ATN (myocardial depressant factor)
releases harmful enzymes
![Page 71: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/71.jpg)
Complications of shock
ARDS: non-cardiogenic pulmonary edema. Increased capillary permeability and interstitial edema. Due to destruction of Type 2 alveolar cells and decreased surfactant production.
Findings: dyspnea: often severe and sudden
Hallmark: decreased PaO2 (< 50 on FiO2 > 40%)
Bilateral diffuse pulmonary infiltrates; decreased lung compliance
PCWP > 18 mm Hg
Treatment: mechanical ventilation with PEEP
Close monitoring of fluid status
Antibiotics
![Page 72: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/72.jpg)
Complications of shock
Acute Tubular Necrosis (ATN): injury may be from ischemia due to renal hypoperfusion or to toxins as seen with sepsis. Treatment: diuretics; improve renal perfusion by fluids or by
increasing cardiac output.
Disseminated Intravascular Coagulation (DIC): Consumptive coagulopathy, microembolization
Findings: prolonged bleeding, oozing.
Decreased platelets, PT/PTT, used all up in clotting
Increased FSP (fibrin split products), released with
breakdown of clot.
Microembolization may lead to multisystem organ failure.
![Page 73: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/73.jpg)
Treatment of Shock
Initiation of Therapy Airway, Breathing, Circulation
Ensure oxygenation and CO2 Removal
Reconstitution of Blood Volume
Evaluate for circulatory disturbances
Focused treatment on circulatory
abnormalities
![Page 74: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/74.jpg)
Treatment of Shock
oxygen delivery:
intubate/ventilate early
![Page 75: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/75.jpg)
Treatment of Shock
fluid replacement: “replace what you lose”
Crystalloids: NS, LR, hypertonic saline
Colloids: albumin, synthetic colloids Non-oxygen carrying colloids
Blood products
Blood substitutes – hemoglobin based oxygen carriers
![Page 76: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/76.jpg)
Treatment of Shock
vasopressors:
Neosynephrine: vasoconstrictor with no chronotropic side effects
Levophed: alpha stimulator
![Page 77: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/77.jpg)
Treatment of Shock
inotropic drugs/IABP
Dopamine 3-20 mcg/kg/min
Dobutamine 2.5-40 mcg/kg/min
antibiotics / drainage
steroids: stabilize cell membranes
![Page 78: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/78.jpg)
Treatment of shock states
Evaluate for different contributing factors.
Initiate therapy with fluid replacement
and evaluate clinical response.
Initiate invasive monitoring if
inappropriate response to volume
replacement occurs.
![Page 79: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/79.jpg)
Bottom line…
Expedient and aggressive
approach to the
patient in shock.
![Page 80: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/80.jpg)
Thank you,
PANA
Go Steelers!!!!
![Page 81: SHOCK STATES - cdn.ymaws.com](https://reader034.vdocuments.us/reader034/viewer/2022050214/626e4d36f04f8640f80090c9/html5/thumbnails/81.jpg)
The End