shock Flashcards

1
Q

Hypovolemic shock

A

decreased CO and PCWP (CVP

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2
Q

Cardiogenic shock

A

decreased CI (or CO)(

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3
Q

Distributive (vasodilatory-“warm or septic shock”)

A

increased CI(> 4.0 L/min/m2) with decreased SVR (

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4
Q

Clinical shock markers

A
  1. SBP 1.0 mmol/L
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5
Q

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?

A

hypovolemic

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6
Q

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)

A

Decreased CVP (normal 0-5 mmHg)

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7
Q

Treatment for Hypovolemic Shock

A

Hypovolemic shock: CVP

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8
Q

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?

A

cardiogenic

CVP > 18 mm Hg and Cardiac Index

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9
Q

Treatment of Cardiogenic Shock

1

A

Upright, O2, Fluid bolus (CVP to 15 -18 mmHg), NIPPV

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10
Q

Treatment of Cardiogenic Shock

2

A

Low BP –dobutamine#(initial 0.5-1 mcg/kg/min with maintenance of 2-20 mcg/kg/min) or milrinone#with intraaorticballoon counterpulsation

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11
Q

Treatment of Cardiogenic Shock

3

A

Normal or high BP –IV nitroglycerin or nitroprusside with IV loop diuretic/furesomide (to relax blood vessels)

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12
Q

Treatment of Cardiogenic Shock

4

A

AF –esmololor cardioversion

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13
Q

Treatment of Cardiogenic Shock

5

A

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)

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14
Q

Treatment of Cardiogenic Shock

6

A

IABP, CABG, or PCI

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15
Q

when treating cardiogenic shock cvp is usually

A

15-18 so use ionotropic agents or vasopressers

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16
Q

dobutamine is best

A

ionotropic

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17
Q

norepi and dopa are good

A

vasopressors

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18
Q

what meds in cardiogenic shock

A

norepi dopa and dobutamine

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19
Q

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

A

pericardial tamponade

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20
Q

electircal alteran

A

every other complex is diffe size it is a marker for pericardia effusion or fluid around the heart

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21
Q

Beck’s triad for Cardiac Tamponade

A

obstructive

  • Distended neck veins
  • Distant heart sounds (bc fluid around heart
  • Distressed BP (Hypotension)
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22
Q

TEE shows an echo free space anterior and posterior to the left ventricular wall. This represents which type of shock?

A

obstructive

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23
Q

Cause of Obstructive Shock

A

Tension pneumothorax

Pericardial disease

Disease of pulmonary circulation (PE)

Cardiac tumor (myxoma)

Left atrial mural thrombus

Obstructive valvular disease

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24
Q

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

A

SIRS

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25
Q

SIRS

A

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

26
Q

SIRS breathing

A

RR > 20 bpm, or PCO2

27
Q

SIRS triad

A

pulse above 90

temp above 38

white count greater than 12000 are the other markers

28
Q

Labs in SIRS, sepsis, or distributive shock

A

CMP

ABGs

Type and crossmatch

Coagulation parameters

Lactate

Blood cultures

29
Q

A gram stain sputum is obtained on the above patient and shows clusters of a gram positive cocci. One may now diagnose

A

sepsis

30
Q

What do the organisms release that cause these patients who are in sepsis to go on to shock?

A

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.

31
Q

Initiation of Host Response in shock/sepsis

A

–Pathogen Associated Molecular Patterns (PAMPs)

–Pattern Recognition Receptors

32
Q

Activation of Pattern Recognition Receptors

A

–MyD88 / NF-kB Signaling
•Pro-inflammatory Cytokines
•Vascular Adhesion Molecules

33
Q

Pro-Inflammatory Cytokines Involved

A

Tumor Necrosis Factor (TNF-a)

IL-1

IL-6

34
Q

Tumor Necrosis Factor (TNF-a)

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
35
Q

IL-6

A

Similar to and redundant of TNF

36
Q

IL-1

A

Similar to and redundant of TNF

37
Q

Sepsis/SIRS

Infection plus:

General variables

any two you have sirs

A

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

38
Q

Sepsis*

Inflammatory variables

A

WBC > 12,000 with bandemia> 10%; WBC

39
Q

Sepsis

Hemodynamic variables

A

SBP*

40
Q

Sepsis

Organ Dysfunction variables

A

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

41
Q

Severe sepsis may be diagnosed in the above patient with evidence of significant dysfunction in how many organs?

A

1

42
Q

Most common evidence of severe organ dysfunction are

A

ARDS, ARF, and DIC; or serum lactate > 4 mmol/L.

43
Q

End-Organ Damage in sepsis

A
–Microcirculatory damage / disorder
•Central Nervous System
•Lungs
•GI
•Liver
•Kidney
44
Q

The above patient is considered to have developed septic shock* when unable to maintain a mean arterial pressure > 60 mmHg after:

A

fluid resuscitation

45
Q

give fluids with

A

septic shock

46
Q

Distributive shock, including septic shock, anaphylaxis, or adrenal insufficiency is characterized by

A

SVR

47
Q

In septic shock a redistribution of oxygen delivery or inability of tissues to extract O2 can actually lead to

A

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

48
Q

with septic shock look for

A

warm skin

49
Q

Early Sepsis Protocol

Nine steps to be done within 2 hours for patients with infection, SIRS, and dysfunction of one organ.

A

give fluids first

  1. Serum lactate
  2. Two sets of blood cultures
  3. Two 18 gauge lines
  4. Start antibiotics
  5. Give 2 liters NS
  6. CBC and BMP
  7. O2 sat > 90%
  8. Start norepinephrine if shock is present.
  9. Transfer for lactate > 4 mmol/L, Systolic BP
50
Q

Septic shock -EGDT

Early Goal Directed Therapy. Problem is O2 utilization (ScvO2)

A
  1. Fluids
  2. Vasopressors
  3. Need to maintain central venous O2saturation at > 70%.
  4. Hope to reduce lactate by 20% in first 2 hours.
51
Q

Fluids for septic shock

A

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.

52
Q

Vasopressors for shock

A

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).

53
Q

heart shock use

A

dobutamine

54
Q

septic shock use

A

norepinephrine

55
Q

Need to maintain central venous O2saturation at > 70%.

A

For

56
Q

Hope to reduce lactate by 20% in first 2 hours.

A

(Increased glycolysis, inhibition of pyruvate dehydrogenase, and impaired liver function, all increase lactate levels)

57
Q

Generally do not transfuse for

A

Hb> 7 gm or hematocrit> 21%

58
Q

Septic Shock

Maintain glucose

A
59
Q

Usual Careversus EGDT

A

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

60
Q

56% of sepsis-related deaths

A

were in people with normal BP and normal or intermediate

serum lactate levels (

61
Q

A patient presents with septic shock. In addition to early recognition and immediate fluid resuscitation:

A
  1. Obtain cultures and remove vascular devices.
  2. 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
62
Q

Renoprotective effect for acetaminophen in severely septic patients

A

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.