shock Flashcards
Hypovolemic shock
decreased CO and PCWP (CVP
Cardiogenic shock
decreased CI (or CO)(
Distributive (vasodilatory-“warm or septic shock”)
increased CI(> 4.0 L/min/m2) with decreased SVR (
Clinical shock markers
- SBP 1.0 mmol/L
A 56 year old alcoholic patient with cirrhosis and ascites presents with vomiting, dry mucous membranes, clammy skin, oliguria, mental status change and BP of 70/50. This patient has which type of shock?
hypovolemic
A 56 year old alcoholic patient with cirrhosis and ascitespresents with vomiting, dry mucous membranes, clammy skin, oliguria, mental status change and BP of 70/50. Which parameter will be found?
A. Decreased CVP (normal 0-5 mmHg)
B. Increased CI (normal 2.0-4.0 L/min/m2)
C. Increased PCWP (normal 4-12 mmHg)
D. Decreased SVR (normal 800-1500 dyne-sec-cm-5)
Decreased CVP (normal 0-5 mmHg)
Treatment for Hypovolemic Shock
Hypovolemic shock: CVP
A 52 y/o female diabetic presents with dyspnea and BP of 65/50. History is positive for an old MI. The patient is on a loop diuretic, an aldosterone antagonist, an ACE inhibitor, and a beta blocker. Heart rate is 140. The skin is cool and clammy and the patient is restless. There are bilateral basilar crackles and the neck veins are distended. This patient most likely has which type of shock?
cardiogenic
CVP > 18 mm Hg and Cardiac Index
Treatment of Cardiogenic Shock
1
Upright, O2, Fluid bolus (CVP to 15 -18 mmHg), NIPPV
Treatment of Cardiogenic Shock
2
Low BP –dobutamine#(initial 0.5-1 mcg/kg/min with maintenance of 2-20 mcg/kg/min) or milrinone#with intraaorticballoon counterpulsation
Treatment of Cardiogenic Shock
3
Normal or high BP –IV nitroglycerin or nitroprusside with IV loop diuretic/furesomide (to relax blood vessels)
Treatment of Cardiogenic Shock
4
AF –esmololor cardioversion
Treatment of Cardiogenic Shock
5
Post MI –antiplatelets, norepinephrine* or dopamine** if hypotensive –MAP to 65 mm Hg) (dobutamine or milrinone#for those with vasoconstriction and not as severe hypotension, ie. BP 80 mm Hg)
Treatment of Cardiogenic Shock
6
IABP, CABG, or PCI
when treating cardiogenic shock cvp is usually
15-18 so use ionotropic agents or vasopressers
dobutamine is best
ionotropic
norepi and dopa are good
vasopressors
what meds in cardiogenic shock
norepi dopa and dobutamine
A 46 y/o female with lung cancer presents with dyspnea and cough. Heart sounds are distant and lungs are clear. Neck veins are distended. BP is 60/40. EKG shows electircal alteran
pericardial tamponade
electircal alteran
every other complex is diffe size it is a marker for pericardia effusion or fluid around the heart
Beck’s triad for Cardiac Tamponade
obstructive
- Distended neck veins
- Distant heart sounds (bc fluid around heart
- Distressed BP (Hypotension)
TEE shows an echo free space anterior and posterior to the left ventricular wall. This represents which type of shock?
obstructive
Cause of Obstructive Shock
Tension pneumothorax
Pericardial disease
Disease of pulmonary circulation (PE)
Cardiac tumor (myxoma)
Left atrial mural thrombus
Obstructive valvular disease
A 25 y/o HIV patient presents with cough, fever of 390C and heart rate of 98 beat/min. Respiratory rate is 26 breaths/min with WBC of 9,000 cells/mm3with 15% bands. Glucose is 145 mg/dL. This patient most likely has
SIRS
SIRS
Dysregulatedinflammation related to autoimmune disorders, pancreatitis, vasculitis, VTE, burns, surgery, etc.
Same category as sepsis
septic immune response syndrome
body is producing cytokines and bacteria are releasing them also
SIRS breathing
RR > 20 bpm, or PCO2
SIRS triad
pulse above 90
temp above 38
white count greater than 12000 are the other markers
Labs in SIRS, sepsis, or distributive shock
CMP
ABGs
Type and crossmatch
Coagulation parameters
Lactate
Blood cultures
A gram stain sputum is obtained on the above patient and shows clusters of a gram positive cocci. One may now diagnose
sepsis
What do the organisms release that cause these patients who are in sepsis to go on to shock?
Pathogen-Associated Molecular Patterns (PAMPs), ie. glycolipids, glycoproteins, lipoproteins, peptidoglycans, lipopolysaccharides, mannoproteins, DNA, RNA, etc. which activate Pattern Recognition Receptors to release cytokines and chemokines and thus produce Shock/MOF/Death.
Initiation of Host Response in shock/sepsis
–Pathogen Associated Molecular Patterns (PAMPs)
–Pattern Recognition Receptors
Activation of Pattern Recognition Receptors
–MyD88 / NF-kB Signaling
•Pro-inflammatory Cytokines
•Vascular Adhesion Molecules
Pro-Inflammatory Cytokines Involved
Tumor Necrosis Factor (TNF-a)
IL-1
IL-6
Tumor Necrosis Factor (TNF-a)
•Stimulates the recruitment and activation of neutrophils and monocytes
–Leads to the production of IL-1
- Activates vascular endothelial cells to express cellular adhesion molecules
- Can induce extrinsic apoptosis
IL-6
Similar to and redundant of TNF
IL-1
Similar to and redundant of TNF
Sepsis/SIRS
Infection plus:
General variables
any two you have sirs
TPR changes –T > 38.3C (101 F) or 90 bpm; RR > 20 bpm or PCO2> 32mmHg
Glucose > 140 mg/dL
Altered mentation
Edema of > 20mL/kg over 24 hours
Sepsis*
Inflammatory variables
WBC > 12,000 with bandemia> 10%; WBC
Sepsis
Hemodynamic variables
SBP*
Sepsis
Organ Dysfunction variables
PaO2/FiO2 0.5 mg/dL(> 2 mg/dL)
INR > 1.5 or PTT > 60 seconds
Ileus
Platelets 4 mg/dL
Hyperprolactinemia> 1 mmol/L (tissue hypoxia)
Decreased capillary refill (tissue hypoxia)
Increased serum lactate
Severe sepsis may be diagnosed in the above patient with evidence of significant dysfunction in how many organs?
1
Most common evidence of severe organ dysfunction are
ARDS, ARF, and DIC; or serum lactate > 4 mmol/L.
End-Organ Damage in sepsis
–Microcirculatory damage / disorder •Central Nervous System •Lungs •GI •Liver •Kidney
The above patient is considered to have developed septic shock* when unable to maintain a mean arterial pressure > 60 mmHg after:
fluid resuscitation
give fluids with
septic shock
Distributive shock, including septic shock, anaphylaxis, or adrenal insufficiency is characterized by
SVR
In septic shock a redistribution of oxygen delivery or inability of tissues to extract O2 can actually lead to
a high central oxygen saturation of
greater than 70%, in the presence of increased serum lactate. Ultimately, however, the CVOS may drop and require fluid, RBCs*,and vasopressors to maintain it above 70
with septic shock look for
warm skin
Early Sepsis Protocol
Nine steps to be done within 2 hours for patients with infection, SIRS, and dysfunction of one organ.
give fluids first
- Serum lactate
- Two sets of blood cultures
- Two 18 gauge lines
- Start antibiotics
- Give 2 liters NS
- CBC and BMP
- O2 sat > 90%
- Start norepinephrine if shock is present.
- Transfer for lactate > 4 mmol/L, Systolic BP
Septic shock -EGDT
Early Goal Directed Therapy. Problem is O2 utilization (ScvO2)
- Fluids
- Vasopressors
- Need to maintain central venous O2saturation at > 70%.
- Hope to reduce lactate by 20% in first 2 hours.
Fluids for septic shock
need to maintain CVP at 8-12 mm Hg. Give 30mL/kg of crystalloid (1-2 liters over 30-60 minutes). May need 4-6 liters total.
Vasopressors for shock
Need to maintain MAP at > 65 mm Hg and cardiac index at 2-4 liters/min2. Use Norepinephrine*5-20 mcg/min (mainly alpha agonist/vasopressor; as is phenylephrine which is pure alpha and therefore good in extreme tachycardia).
If norepinephrine fails, go to epinephrine(mainly beta agonist/inotropic effect). May also consider Vasopressin 0.03 units/min (potentiates norepinephrine).
heart shock use
dobutamine
septic shock use
norepinephrine
Need to maintain central venous O2saturation at > 70%.
For
Hope to reduce lactate by 20% in first 2 hours.
(Increased glycolysis, inhibition of pyruvate dehydrogenase, and impaired liver function, all increase lactate levels)
Generally do not transfuse for
Hb> 7 gm or hematocrit> 21%
Septic Shock
Maintain glucose
Usual Careversus EGDT
The treatment of septic shock should be based on Usual Care in deference to Early Goal Directed Therapy (EGDT). In other words, provider directed usual care is as good as EGDT, if based on rapid recognition,* early antibiotics, and aggressive fluid resuscitation. This rather than necessarily placing central line for CVP and CvO2
56% of sepsis-related deaths
were in people with normal BP and normal or intermediate
serum lactate levels (
A patient presents with septic shock. In addition to early recognition and immediate fluid resuscitation:
- Obtain cultures and remove vascular devices.
- Begin vancomycin (may use daptomycin, linezolid, or ceftaroline) and cefotaxime(may use cefotetan, cefepime, cefoperazone, ceftazidime, pipericillin-tazobactam, ticarcillin-clavulanate, meropenem, or imipenem). Must cover MRSA, Pseudomonas, and Gm negatives with ESBLactivity
Renoprotective effect for acetaminophen in severely septic patients
No long-term benefit of adrenaline in cardiac arrest outside the hospital –contracts vessels in gut, liver, and kidneys. On the other hand, faster administration of epinephrine(one to three minutes) in people who arrest in the hospital with a non-shockablerhythm (asystole or PEA) have increased survival.
