Shock

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1.

4 ways to arrive at cellular hypoxia

(shock)

hypovolemia, cardiac dysfunction, vascular failure,

or obstructive processes that impair cardiac filling.

2.

big overview of shock (key point, Dx,

etc)

A state of organ hypoperfusion with resultant cellular dysfunction and

death.
Mechanisms may involve decreased circulating volume, decreased cardiac
output, and vasodilation, sometimes with shunting of blood to bypass
capillary exchange beds.
Symptoms include altered mental status, tachycardia, hypotension, and
oliguria.
Diagnosis is clinical, including BP measurement and sometimes markers
of tissue hypoperfusion (eg, blood lactate, base deficit).
Treatment is with fluid resuscitation, including blood products if
necessary, correction of the underlying disorder, and sometimes
vasopressors.

3.

pro tip: it's important to recognize

when shock is coming!

...

4.

Shock- Pathophysiology

Reduced perfusion -> hypoxia -> anaerobic metabolism

Lactic acidosis -> cell damage -> cell death
Inflammatory and clotting cascades triggered
cytokines, leukotrienes, tumor necrosis factor, Nitric oxide ("cytokine storm" in influenza A,
H1N1)
Vasodilation -> hypotension -> hypoperfusion
Leukocyte and platelet adhesion to endothelium
clotting system activation with fibrin deposition
Endothelial cell dysfunction -> inc microvascular permeability (causes microvascular
permiability, leads to third space, leads to hyptension)
third space, translocation of enteric bacteria (gives peritonitits)
Neutrophil apoptosis inhibited -> increases inflammatory mediators
(shock is overwhelming display of force)
PRO TIP -- so not only do we need to think about fluids, but a ton of other things.

5.

pathophysiology cont.

Compensation
inc oxygen extraction
adrenergic and sympathetic mediated
vasoconstriction and tachycardia
inc cardiac output
release of corticosteroids, renin, glucose

6.

Graphic Organizer

7.

multiple organ dysfunction

Most common in septic shock

10% of pts with severe traumatic injury
Lungs
inc membrane permeability
alveoli dysfunction and inflammation
hypoxia, acute lung injury, ARDS
Kidneys
acute tubular necrosis -> ARI
Heart
dec. contractility and compliance
dec. cardiac output
GI tract
ileus, submucosal hemorrhage, hepatocellular
necrosis, dec. production of clotting factors

8.

shock sxs

Lethargy, confusion, and somnolence are common.

Pale, cool, clammy, and often cyanosis
earlobes, nose, and nail beds.
capillary filling time is prolonged
Diaphoresis
Peripheral pulses are weak and rapid (Kuhn likes to feel radial pulse);
only femoral or carotid pulses are palpable.
Tachypnea and hyperventilation
BP low (< 90 mm Hg systolic) or unobtainable
Urine output is low.

9.

shock index (used in trauma, used

to clue us into shock)

Shock Index
hypovolemic shock
HR / SBP (HR divided by systolic BP)
0.5 - 0.7 normal

SIRS (also used) (systemic

inflammatory response syndrome)

Temperature <36C(96.8F) or >38C

(100.4F)
Heart rate >90 beats per minute
Tachypnea > 20 breaths per minute
White blood cell count <4000 cells/mm
or >12,000 cells/mm or the presence of
greater than 10% immature neutrophils
(band forms)
2 OR MORE CRITERIA PRESENT (should lead to evaluation to make sure)

10.

SIRS

Infectious and Noninfectious

Sepsis
Trauma, burns, pancreatitis, ischemia, and hemorrhage
Complications of surgery
Adrenal insufficiency
Pulmonary embolism
Complicated aortic aneurysm
Cardiac tamponade
Anaphylaxis
Drug overdose

11.

HYPOVOLEMIC SHOCK

Decrease in intravascular volume, decreased preload > reduced stroke volume.

* Hemorrhage
Increased losses body fluids
Inadequate fluid intake

12.

Signs of Successful Resuscitation

1.
2.
3.
4.
5.
6.

13.

Hypovolemic Shock- Treatment

Stop bleeding or fluid loss

Crystalloid infusion 20cc/kg IV bolus which is a good couple liters (lactated ringers...most use
normal saline except in someone hypovolemic due to renal failure?!?!)
no advantage to colloids (eg, albumin, blood is a colloid)
Reassessment
Massive transfusion protocols
PRBCs : FFP : Platelet : cryoprecipitate (I think he said that now they do a 1:1:1:1 kinda thing)

14.

CARDIOGENIC SHOCK

Reduction in Cardiac Output

primary cardiac disorder

Improved blood pressure

Improving level of consciousness
Improving peripheral perfusion
Decreasing tachycardia
Decreasing lactate
Normalizing pH

15.

Cardiogenic Shock Tx:

Cardiogenic Shock- Treatment

Tachydysrhythmias- cardioversion
Bradydysrhythmias- pacing
STEMI- revascularization
Supportive: ASA, O2, Heparin
Vasopressors (for hypovolemic shock): Norepinephrine,
Dobutamine,
Dopamine

16.

pro tip: when you see multiple organ failure....TREAT

AGGRESSIVELY

...

17.

Pro Tip: 3 most common 'pressors >>

Norepinephrine,
Dobutamine,
Dopamine

18.

Vasoactive receptors

Alpha-1 adrenergic receptors

sympathetic nerve endings on smooth muscle cells and
on myocardial cells
Alpha-2 adrenergic receptors
systemic vasculature leads to vasoconstriction and
increased systemic blood pressure
1 and 2-adrenergic receptors
both located within the myocardium
2 receptors also being located vascular and bronchial
smooth muscle.
positive ionotropic and chronotropic effects within the
myocardium
smooth muscle relaxation in the bronchial tree and
elsewhere
Dopamine receptors
smooth muscle of renal, splanchnic, coronary, and '
cerebrovascular beds
vasodilation within these vascular beds

19.

drugs affecting which receptors

(i think he said norepinephrine is the go to in ED)

20.

DISTRIBUTIVE SHOCK

Distributive Shock
Dec. intravascular volume caused by arterial
or venous vasodilation
Anaphylaxis
Endotoxin induced sepsis
Spinal cord injury
Drugs: nitrates, opioids, Viagra

21.

ANAPHYLACTIC SHOCK (remember this is on a spectrum)

Airway: angioedema and bronchospasm

EpiPen
Beta- agonist aerosol (albuterol is most common)
H1 and H2 blockers (H1...benadryl.....H2 ranitidine)
Steroids (prednisone...classic orally....dexamethasone for
kids.....sodium hydrol IV?!)

22.

NEUROGENIC SHOCK (high thoracic or cervical injury..........legs

and or arms can't move)

Loss of vascular tone from high spinal lesion

loss of feedback loop from autonomic ganglia
Warm skin, hypotension, +/- tachycardia
Fluids and vasopressors with alpha activity

23.

SEPTIC SHOCK (Key

points)

SIRS
Temperature <36C(96.8F) or >38C(100.4F)
Heart rate >90 beats per minute
Tachypnea > 20 breaths per minute
White blood cell count <4000 cells/mm or >12,000 cells/mm or the presence of greater than
10% immature neutrophils (band forms)
2 or more criteria present
SIRS + infection = sepsis
Sepsis + organ dysfunction = severe sepsis
Sepsis + cellular hypoxemia = septic shock

24.

septic shock (points)

SIRS associated with decreased SVR -> hyperdynamic compensation ->

impaired contractility from myocardial depressants and hypoxemia.
Elevated serum lactate levels (> 4) evidence of tissue hypoperfusion.
Gram-negative rods (classic....E Coli...Pseudomonas)
Fluids!!! (eg, 3 liters of fluid for the little old lady exampe.....in ER it's common to get 3 or 4 liters for
sepsis mgmnt. Much more than you'd think is normal)
Antibiotics --- early antibiotic, broad spectrum, even if it's the wrong one just do it and kinda hope you get
lucky
Steroids (maybe...that is, some do and some don't)
Early goal directed therapy

25.

OBSTRUCTIVE SHOCK

Mechanical factors that interfere filling or

emptying of the heart or great vessels.
tension pneumo, cava compression, cardiac tamponade, atrial tumor or clot (mechanical interference with
ventricular filling)
Interference with ventricular emptying (PE)

26.

obstructive shock (Tx),

Tension Pneumo

Tension pneumothorax
dec breath sounds, tracheal deviation
respiratory distress and shock
needle decompression

27.

Tx: pericardial tamponade

Pericardial tamponade
hypotension, JVD, muffled heart sounds
Beck's triad
Pericardiocentesis
(Best way to Dx is ultrasound)
* Not that common

28.

Tx: Massive PE

Chest pain, syncope, tachypnea, hypotension

JVD, RV strain on EKG (and seen on echo)
Surgical embolectomy
Thrombolytics
TPA works great for pt with large PE (not small or moderate PEs though) Also given to Pt in shock. Kuhn
says he's seen TPA work in about 30 min. IV.

"very common"

29.

summary points

A state of organ hypoperfusion with resultant cellular dysfunction and

death.
Mechanisms may involve decreased circulating volume, decreased cardiac
output, and vasodilation, sometimes with shunting of blood to bypass
capillary exchange beds.
Symptoms include altered mental status, tachycardia, hypotension, and
oliguria.
Diagnosis is clinical, including BP measurement and sometimes markers
of tissue hypoperfusion (eg, blood lactate, base deficit).
Treatment is with fluid resuscitation, including blood products if
necessary, correction of the underlying disorder, and sometimes
vasopressors.