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Flashcards in shock Deck (69)
1

what is shock

Impaired O2 delivery/utilization

Increased O2 consumption

asymmetry in supply and demand

2

why do we care about shock

hypo-perfusion

When it becomes irreversible (cells start to die) > multi-organ failure and death

3

what decreases supply

Pump failure

Decreased total blood volume

Poor vascular tone (vessels can’t be leaky)

4

What can increase demand?

Exercise
Infection
Meds/toxins
Hypermetabolic states (hyperthyroidism, pregnancy, anemia)

5

poor vascular tone

leaky blood vessels

6

kidney failure looks like

increase in Cr

fluid retention
(urine output is decreased)

might need a catheter

7

loss of perfusion to the brain looks like

altered mental state
agitation
loc
confusion
intracerebral bleeding
coma

8

loss of perfusion to the lungs can result in

acute respiratory distress

9

drugs that cause shock

prescription medications
toxins

10

BP

CO times SVR (systemic vascular resistance)

11

co

SV (amt of blood you are pushing out)

times HR

12

anaphylaxis and toxins have a direct effect on

SVR (systemic vascular reserve)

13

What happens when we don’t have O2

We go through the process of fermentation. We get a build up of lactate

14

what happens when you get a lactic acid build up?

You get lactate build up bc it disrupts the electrolyte balances in the cell. We see influx of Ca++ and it triggers a process called apoptosis.

15

respiratory complications of

tachypnea
SOB
can go into ARDS
(lungs fill with fluid and lungs are crying bc they are not getting enough oxygen),

16

The normal blood lactate concentration in unstressed patients is

0.5-1 mmol/L.

something around 2

17

Early sign shock

MAP decreased 10 mmHG

effective compensation

O2 is still getting to vital organs and

increased heart rate

18

what are compensatory signs

MAP down 10-15 mm Hg
increased RENIN and ADH

-->vasoconstriction

decreased PP
increased HR
decreased pH
restless
apprehensive

19

progressive signs (intermediate)

decreased MAP 20 mm Hg

tissue organ hypoxia
decreased UO
decreased pH
weak rapid pulse

sensory changes

20

refractory signs irreversible

excessive cell organ damage

multisystem failure and decreased pH

21

this is where you start to see cellular damage. Kidneys start to fail

Progressive signs of shock

22

Coagulation of shock

PT/INR will be elevated, DIC is present (purpura, INR will be through the roof)

23

effect on kidneys

decreased urine output, get creatinine

24

cardiac markers of shock

tachycardia, chest pain, EKG disturbances

25

Liver effects

hypotensive, LFTs (AST/ALT in the 1000s --> this is shock liver), bilirubin and albumin can be high

26

your vascular tone is failing (leaky blood vessels)

i. Distributive shock

27

Distributive shock what is happening

Something is telling them to dilate and it causes leakage of nutrients into the interstitium. So even though your blood volume is good, your blood vessels are leaky so they are not getting the nutrients

SUPPLY

28

hypovolemic

not enough gas in your tank. Pump is working and vascular tone is good but don’t have enough volume

SUPPLY

29

Cardiogenic shock

DEMAND

pump failure can't get the blood where it needs to be

NO FLUIDS

fluid in lungs--> need to intubate--> sedation drops pressure--> coding

30

obstructive shock

SUPPLY
everything is working but there is something blocking and you're not getting O2

31

peritoneal signs of hypovolemic shock

rigid abdomen

blood is irritating

32

hemorrhagic hypovolemic shock can look like

• Trauma
• GI Bleed
• AAA rupture
• Ruptured ectopic pregnancy (call the OB)
• Post-partum hemorrhage

33

hypovolemic tx can look like

pressor
fluids
blood

34

Non-hemorrhagic causes of hypovolemic (4)

• GI loss (vomiting/diarrhea)
• Inadequate intake
• Environmental/neglect
• Burns

35

if you loose 700 mL of blood or 15% BV you are what class of shock

class I

normally HR increased

36

class 3 of shock

1500-2000
loss of 30-40% BV
HR >120
RR 30-40
decreased systolic blood pressure
urine output decreased
5-15 mL

37

class 2 of shock

750-1500
15-30%
>100
20-30 rr
NORMAL bp

20-30mL UO

38

class IV of shock

>2000 mL
>40%
>140
>35 RR
greatly decreased systolic BP
UO minimal

39

in hypovolemic shock you want to start IV with a

crystalloid

maybe colloid for cardiac and pulmonary complications

40

TX of hypovolemic shock

1. ABCs
2. Good IV access
3. VOLUME – start with crystalloid
4. Blood if bleeding (massive transfusion protocol)
5. Pressors - Norepinephrine
6. Definitive management (stop bleeding, OR/endoscopy if needed, treat underlying condition)

41

71 y/o M, hx of HTN, DM, prior stents with CP/SOB/dizziness/weakness for the last 5 hours


VS: 96.2 104 72/50 27 91% 4L NC


what type of shock would you suspect

i. Ill appearing, dyspneic
ii. Tachycardic
iii. Crackles in both lungs
iv. 2+ pitting edema to knees bilaterally

cardiogenic shock picture

need an ECG
bedside echo

42

causes of cardiogenic shock (5)

MI or infarction
valvular disease
cardiomyopathy
myocarditis
toxins

43

Tx of cardiogenic shock

i. ABCs (C also for Call Cardiology!!)
ii. Oxygenation/Intubation
iii. IV access
iv. Careful fluid resuscitation
v. Inotropes/Vasopressors (Dobutamine/Norepinephrine)
vi. Definitive management (cath lab for stent/balloon pump vs. OR for CABG/valve replacement)

44

a. A 23 y/o healthy M presents with weakness, chills, nausea and abdominal pain for 3 days

b. VS: 103.2 117 71/45 22 100% on RA
c. Exam
i. Ill appearing, +rigors
ii. Dry MM
iii. Abdomen uncomfortable to palpation, particularly in the lower quadrants, +rebound/guarding


i. WBC 29
ii. Creatinine 2.9
iii. Lactic acid 4
iv. UA: no signs of infection

distributive shock

45

WBC normal

4.5-11

46

normal creatinine

.8-1.4

47

reasons for distributive shock

septic shock
anaphylactic shock
neurogenic shock

48

what is the reason for septic shock

Overwhelming systemic infection

49

common causes of Anaphylactic shock

a. Food
b. Medication
c. Contrast
d. Insects

50

reasons for neurogenic shock

spinal cord injury is an example

51

in general how should we treat distributive shock

• ABCs
• IV access
• Fluids
• Vasopressors (Norepinephrine)

52

septic shock tx

• Look for source!
• Antibiotics (broad)
• Source control (surgery if needed)

53

anaphylactic shock tx

• Epinephrine (0.3mg IM)
• Steroids
• H1/H2 blockers
• Decontamination

54

neurogenic shock tx

• C collar/stabilize spine
• Atropine/pressors
• Steroids controversial
• NSG intervention

55

what would obstructive shock look like on a ecg

on CXR

on echo

low voltage

CXR shows – cardiomegaly

ECHO shows --- large pericardial effusion w/ cardiac tamponade

56

causes of obstructive shock

1. Cardiac tamponade
2. Tension pneumothorax
3. Pulmonary embolism
4. Severe aortic stenosis

57

how does Cardiac tamponade create shock

TX

Tamponade = can’t fill the heart

Obstruction = pericardial effusion

• Pericardiocentesis

58

how does tension pneumothorax cause shock

can’t fill the heart

Obstruction = air in chest; with mediastinal shift and tracheal deviation

• Chest tube

59

Pulmonary embolism as a cause of shock

can’t fill the heart
a. Obstruction = large clot in PA

• Thrombolytics/anticoagulation

60

Severe aortic stenosis

can’t pump out into aorta
a. Obstruction = stenotic aortic valve

• Valve replacement

61

what does a pt in shock look like ?

i. Ill appearing
ii. Abnormal vitals (hypotension, tachycardia)
iii. Weak pulses
iv. Mental status changes
v. Cool/clammy extremities

62

what does assessment look like in a pt with shock

i. BP (?Art line/central line for CVP)
ii. Lactate clearance
iii. Hemoglobin (>10)
iv. Urine output (>0.5 ml/kg/hr)

63

SNS neurotransmitters

noraderenaline and adrenaline

64

B1 receptor

both increases heart rate and contractility and speed

65

B2

stimulation leads to vasodilation

66

A1

stimulation causes vasoconstriction

67

catecholamine release that in response to a drope in CO

epinephrine
norepinephrine

68

septic shock

LPS toxins cause

nitric oxide release from cell damage

compliment cascade triggered causing mor vasodilation

TNF causes more release of inflammatory chemicals

damagining the endothelial cells and making them leaky

procoagulant-TF also released leads to clotting and bloackages and further decreased profusion

69

how does distributive shock look different

MVO2 shock can be normal