3 Shock, Sepsis, MODS & DIC (part 1) Flashcards

1
Q

Shock
-definition
-results from ?
-progresses to what 2 things?

A

Inadequate tissue perfusion
Imbalance between oxygen supply and demand

Results from:
-ineffective cardiac function
-inadequate blood volume/vascular tone

Progresses into SIRS and MODS

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2
Q

4 systems that work together to maintain homeostasis in shock

What happens if 1 fails

What happens if 2 or more fails

A

Blood volume
Myocardial contractility
Blood flow
Vascular resistance

When 1 fails others work to compensate

When 2 or more fail we have SHOCK

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3
Q

Stages of shock (4)

A

Initiation
Early/compensatory (reversible)
Progressive (intermediate)
Irreversible (refractory)

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4
Q

Stage 1 of shock

Initiation (reversible)

A

-decrease tissue oxygenation

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5
Q

Stage 2 of shock

Early/Compensatory
(Body starts to compensate)

Neural compensation by what?

A

Neural compensation by SNS (fight or flight):

—increased HR/contractility/vasoconstriction
—redistribution of blood flow from nonessential organs to essential organs
—bronchodilation

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6
Q

Stage 2 of shock

Early/Compensatory

Endocrine compensation

A

RAAS, ADH, glucocorticoids released
(Renin angiotensin aldosterone system):

—vasoconstriction

—renal reabsorption of Na, Cl and water

—converts glycogen to glucose for energy

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7
Q

Stage 2 of shock

Early/Compensatory

Chemical compensation

A

Chemical receptors increase rate/depth of breathing :

=hyperventilation

=alkalosis

=vasoconstriction of cerebral blood vessels

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8
Q

Stage 2 of shock

Early/Compensatory

Clinical manifestations

A

SNS:
Increased HR (except neurogenic shock)
Narrowed pulse pressure
Rapid deep resp (causes alkalosis)
Thirst
Oliguria (increased specific gravity)
Decreased bowel sounds
Hyperglycemia

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9
Q

Stage 3 of shock
(Failure of compensatory mechanisms)

Physiologic events:

A

Tissue hypoperfusion

=aerobic to anaerobic metabolism

=lactic acidosis

Resp/metabolic acidosis
(Inadequate Na/K pump)

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10
Q

Stage 3 of shock
(Failure of compensatory mechanisms)

Clinical manifesations

A

Hyper/hypoglycemia
Dysrhthmias
Anuria (increased BUN/creatinine/potassium)
Decreased BP
Lethargy to coma
Absent bowel sounds
Tachypnea

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11
Q

Stage 4 of shock
(Refractory)

Physiologic events

A

-Severe tissue hypoxia
-tissue necrosis
-worsening acidosis

(SIRS/MODS)

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12
Q

Stage 4 of shock
(Refractory) (NONREVERSIBLE)

Clinical manifestations (everything starts to fail)

A

-dysrhuthmias
-severe HOTN despite pressors
-acidosis
-acute resp failure
-DIC/liver failure
-AKI
-MI
-cerebral ischemia/infarction

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13
Q

4 classifications of shock

A

Hypovolemic (inadequate volume)

Cardiogenic (inadequate contractility)

Obstructive (obstruction of blood flow)

Distributive (inadequate vascular tone)
-anaphylactic/neurogenic/septic

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14
Q

Hypovolemic shock

Clinical manifestation:
What happens to HR/RR/BP/CVP/PAOP/SVR

Management: 3 things to look at

A

Increased HR/RR/SVR

Decreased BP/CVP/PAOP

Management:
-UOP 30ml/hr
-CVP 2-6
-SBP over 90/ MAP over 65

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15
Q

Hypovolemic shock causes (basic level)

A

Loss of fluids (blood/burns/v/d/diuresis)

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16
Q

Hypovolemic shock
Lab findings

A

Serum lactate (1.2) increased
= lactic acidosis (decreased perfusion)

—ABG/electrolytes
—H&H
—Decreased SvO2 (<60%)
-all shock is low SvO2 d/t decreased perfusion

17
Q

Hypovolemic shock tx

-IV needed
(Do what with what solutions)

A

Fluid resuscitation
-multiple large bore IVs

Crystalloid solution (isotonic)
Blood products
Other colloid solutions (albumin/ volume expanders)

18
Q

Hypovolemic shock tx

How fast to replace fluids
-what type of line to measure what?

Worries about giving large amounts of blood

Continuous resp assessment to watch for what 2 things?

A

1-2L (crystalloid solutions) over 10-15mins

Central line w/ CVP capability

Worries: hypocalcemia from citrated plasma

Continuous resp assessment:
-pulmonary congestion
-resp distress thru inadequate oxygenatioln

19
Q

Cardiogenic shock

Causes

Clinical manifestations
-what happens to HR/RR/BP/SvO2/CVP/PAOP
(What does it look like)

-other 1 symptom

A

All heart issues (HF/MI/cardiomyopathy)

Symptoms (look like a active MI)
Increased HR/RR
Opposite of hypovolemic (increased CVP/PAOP)
Decreased SvO2, BP

Chest pain

20
Q

Difference between hypovolemic shock and cardiogenic shock

A

hypovolemic (decreased CVP/PAOP)

Cardiogenic (increased CVP/PAOP)
—Cardiogenic is heart issue but not a volume issue like hypovolemia

21
Q

Cardiogenic shock management

Goal:
3 things to do/give
2 machines we can put them on
1 procedure we can do

A

Goal: improve contractility:
-inotropic agents (dopamine, dobutamine)
-keep MAP >65
-reduce preload and afterload (CVP/PAOP)

Put on:
Ventilator
IABP

Procedure:
Cath lab (improve blood flow)

22
Q

Cardiogenic shock labs

A

Increased in MI:
—CPK-MB
—Troponin

Increased if increased myocardial pressure:
—BNP

23
Q

Cardiogenic shock tx:

Goal:

A

Decrease myocardial workload

Increase myocardial oxygen delivery

24
Q

Cardiogenic shock meds

5

A

ACE inhibitors
ARBs
Diuretics
Digoxin

Dobutamine:
-B1 and B2 agonist
-Increases CO and decreases PAWP

25
Obstructive shock causes 3 1st has 3 2nd has 2 3rd has 3
—something stops flow to heart Impaired diastolic filling: -cardiogenic tamponade -tension pneumothorax -constrictive pericarditis Increased right ventricular afterload: -pulmonary HTN -PE Increased left ventricular afterload: -aortic dissection -aortic stenosis -HTN
26
Obstructive shock Clinical manifestations -what happens to HR/RR/BP/PAOP/SVR
Increased HR/RR/PAOP/SVR Decreased BP
27
Obstructive shock management/tx
Cardiac tamponade: —pericardiocentesis PE: —anticoagulants Tension pneumothorax: —chest tube
28
Distributive (vasogenic) shock Characteristics (2)
Vasodilation —Decreased peripheral vascular resistance
29
Distributive (vasogenic) shock -3 common causes
Neurogenic (SNS) Anaphylactic: -histamine = vasodilation Septic
30
Distributive: neurogenic shock Causes Clinical manifestations -main symptom -what happens to BP and why
Causes: —upper SCI —spinal anesthesia —neuromuscular blocking agent -Decreased HR (bradycardia) -Vasodilation = low BP
31
Distributive: neurogenic shock Tx
Atropine: -for symptomatic bradycardia Vasopressors -for low BP
32
Distributive: anaphylactic shock What happens to HR/RR/BP/UOP
Increased HR/RR Decreased BP/UOP
33
Distributive: anaphylactic shock Tx
Maintain airway Vasopressors for BP: Epinephrine
34
Distributive: septic shock Tx
Fix Vasodilation: —IVF resuscitation —Vasopressors (norepinephrine) —abx
35
SIRS (systemic inflamation response syndrome) -4th stage = any shock can cause it) -what is happening -3 other things that happen -SIRS does not mean pt has what?
Widespread inflammation: —increased capillary permeability —-fluid shifts intravascular to interstitial spaces ——hypovolemia from fluid shift (Microvascular clotting/impaired fibrinolysis/vasodilation) SIRS does not mean pt has sepsis and doesnt always lead to sepsis (their seperate things)