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Trauma Surgery [SHOCK]

Introduction Unconscious (GCS<8) Expanding Talking in full

Whenever dealing with a trauma patient, the priorities are the Gurgling Hematoma sentences

ABCs: Airway, Breathing, Circulation - in that order. Without a Stridor

patent airway air is unable to move with breaths. Without Cutaneous Coughing

breathing it’s impossible to deliver oxygen or remove CO2 - Emphysema Good Air Movement
there’s no point in having circulation. Therefore, the first step

should be the evaluation of the airway. Managing the Airway

1) Airway: an airway is considered patent if the patient is OPA Avoid OPA in gag reflex

talking, coughing, or moving air. If the patient is NPA Avoid NPA in facial fracture
gurgling (blood or fluid), there’s stridor (laryngeal ET Tube Preferred Definitive Method

edema), or has no air movement (apnea), then we must NT Tube Avoid in facial fracture

intervene. A patient may appear stable but requires Cricothyroidotomy If ET Fails, temporizing

prophylactic intervention in the case of an expanding Tracheostomy Only in OR, Definitive

hematoma or severe trauma. An airway is assessed with

a head-tilt chin-lift and secured with an endotracheal Breathing

tube or with cricothyroidotomy. Emergent tracheostomy Monitor SpO2, ET-CO2

should NOT be attempted in the ER, only in the OR. Intervene With BVM, Ventilator, Oxygen

2) Breathing: if there are bilateral breath sounds the patient

is breathing adequately. A BVM or ventilator may be Circulation

needed to assist ventilations. Monitor breathing with Shock = SYS BP < 90 or Uoutput<0.5mL/kg/hr

pulse oximetry and/or end-tidal capnography.

3) Circulation: shock is defined by any number of Type Physical Path Tx

parameters. A Systolic Blood Pressure < 90 or Urine Hemorrhagic Flat Veins, Active IVF, Blood,
Output < 0.5mL/kg/hr or clinical signs of shock (pale, Clear Lungs Bleeding Surgery

cool, diaphoretic, sense of impending doom) is Tamponade Engorged Blunt Chest Pericardiocentesis

sufficient to diagnosis shock. Veins, clear Trauma Pericardial

Shock Lung Sounds Window

Shock in the traumatic setting has one of three causes. Tension Engorged Penetrating Needle to
1) Hemorrhage drains the tank. There is a hole somewhere Pneumo Chest Trauma Chest Tube

that needs to be plugged. The patient will have flat veins Sounds

and rapid HR to compensate. The most important thing Cardio Engorged Massive MI Inotropes

to do is plug the hole in the OR. However, there may be genic Veins, Lung
transport time or prep time before the hole can be Sounds

closed. In the meantime, start 2 large bore IVs (> 16 G) Flushed, Pink, Spinal Trauma Vasopressors
Vasomotor

and run fluids. First LR then Blood as it becomes Warm or Anesthesia

available. See Resuscitation and Location to the right. Septic Flushed, Pink, Sepsis Vasopressors and

2) Tamponade is caused by severe blunt trauma that Warm Abx

reduces cardiac filling. Blood backs up into the venous

system so the patient presents with distended Neck Veins

but clear lung sounds. Emergent pericardiocentesis

(ER) or mediastinotomy/thoracotomy (OR) is required. Hemorrhagic Resuscitation

3) Tension Pneumothorax is caused by penetrating

trauma and fills the pleural space with air or blood,

(1) Direct Pressure
(2) Elevate Extremity

compressing the veins feeding the heart. There are

(3) Arterial Tamponade

distended neck veins (like in tamponade) but there are

(4) Tourniquet

reduced lung sounds on the affected side and tracheal

(5) 2 Large G IVs IO
deviation away from the lesion. Emergent needle

decompression and chest tube (thoracostomy) is

(6) IVF (Crystalloids)
(7) Blood

required.
(8) Surgery

Airway Do not be confused by some of the causes of non-traumatic shock

Intervene Now Intervene Soon No Intervention

© OnlineMedEd. http://www.onlinemeded.org


Trauma Surgery [SHOCK]

1) Cardiogenic shock occurs after a major MI and is a

product of pump failure. Forward flow fails so blood

backs up. There will be bilateral pulmonary edema and

distended neck veins. This is the major differential

against tamponade and tension pnuemo. Giving fluids can

be fatal while the treatment is actually inotropes. Don’t

get tripped up.

2) Vasomotor shock is loss of sympathetic tone that keep the

arteries constricted. There’s massive vasodilation

everywhere; suddenly the tank is too big to be filled by

what’s in the body. This occurs in spinal trauma or

anesthesia. The patient will be pink, warm and dry with

a low BP. Give back the tone with vasopressors and

correct the underlying problem.

3) Septic. Local cytokines increase blood flow (leukocyte

delivery) and increase vascular permeability to fight local

infection. Cytokines everywhere cause a variant of

vasomotor shock, resulting in vasodilation (warm, pink,

and dry). Identify the organism with blood cultures and

treat with both vasopressors and antibiotics.

© OnlineMedEd. http://www.onlinemeded.org


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Shock
Jason Ryan, MD, MPH
Shock
Life-threatening fall in blood pressure
Poor tissue perfusion
Low cardiac output
Loss of contractility
Low intravascular volume
Peripheral vasodilation

BP = CO X TPRperipheral
totalresistance
Types of Shock
Cardiogenic
Cardiac disorder fall in cardiac output
Hypovolemic
Fall in intravascular volume fall in cardiac output
Hemorrhage
Distributive
Peripheral vasodilation
Capillary leak
Septic, anaphylactic
Obstructive
LPE teafonade
Types of Shock
Different treatments for different types of shock
Often can determine type from history
Myocardial infarction cardiogenic shock
Massive bleeding hypovolemic shock
Shock of unclear etiology: Swan-Ganz catheter
Swan-Ganz Catheter
Pulmonary artery catheter

TA
RA A
Pulmonary Capillary Wedge Pressure
PCWP

Equal to LA pressure

Pressure
RU poop is
ttat
Timed.fm
 A i i i N I i n t c

Swan-Ganz Data
RA pressure: normal ~ 5 mmHg

f
RV pressure: 20/5
PA pressure: 20/10
the normalbaling
PCWP: 10
Mixed venous O2 sat: 65-75%
Mixed
venom Oxygen concentration after all veins mix
Falls with low cardiac output
oxygen
content
Fick Equation
Oxygen Consumed = O2 Out Lungs O2 In Lungs
= CO (Art O2 Ven O2)

Cardiac Output = O2 Consumption

(Art O2 Ven O2)

O2 Consumption body size

Arterial O2 Content = O2 sat on finger probe
Venous O2 Content = O2 from Swan-Ganz

Swan-Ganz catheter gives cardiac output

Flow Equation
Used to determine total peripheral resistance (systemic vascular resistance)

MAP RAP = CO * TPR

Rightatrial
pressure
TPR = MAP RAP
I CO

Swan-Ganz Catheter gives TPR

 Swan-Ganz Data
Direct
RA pressure: normal ~ 5 mmHg
RV pressure: 20/5
PA pressure: 20/10
PCWP: 10
Mixed venous O2 sat: 65-75%
Calculated
I Cardiac output
Total peripheral resistance/systemic vascular resistance (SVR)

indirectly
U thing
same
Hemodynamics of Shock
Four major classes of shock
Cardiogenic
Hypovolemic
Distributive
Obstructive
All have different hemodynamics
Swan-Ganz catheter can be used to determine etiology of shock
Cardiogenic Shock
Low cardiac output NCO.IR
High cardiac pressures
High SVR (sympathetic response)
Classic cause: large myocardial infarction
Also seen in advanced heart failure (depressed LVEF)
Treatment: inotropes
Dobutamine
Milrinone
Do not give fluids!
Hypovolemic Shock
f co gsur dcardiac Pressures Rap etc
Low cardiac output
Low cardiac pressures
High SVR (sympathetic response)
Poor fluid intake
High fever, insensible losses
Hemorrhage Tose morewater throughlung andbreathing
Treatment: fluids or blood transfusion
Distributive Shock
Hallmark only one with low sur
Low SVR
Diffuse vasodilation and/or endothelial dysfunction
Sepsis (most common)
Anaphylaxis
Cardiac output classically high (but variable)
Depends on degree of capillary leak

f
Cardiac pressures also variable

no need to know.
Distributive Shock
Treatment based on cause
Septic shock: fluids, antibiotics, vasopressors
Anaphylaxis: epinephrine
 A fra T afreeh.com for more

Type of Shock
Wtl Cardiogenic Hypovolemic Distributive

F Blood Pressure
HR
RA/RV/PCWP
on'VE
-
Cardiac Output
SVR

only one
Major Shock Types
SVR
SUR

part t
Low
High

Distributive
Pressures

High Low

Cardiogenic Hypovolemic
Physical Exam and Labs
Cold skin poor perfusion
High SVR and low CO
Cardiogenic
Hypovolemic
Warm skin good perfusion
Low SVR and high CO
Distributive
Elevated serum lactate
nonspecific
Public Domain

finding
seen in all forms ofshock
Physical Exam and Labs
Jugular venous pressure high RA pressure cardogenic
Pulmonary rales high LA pressure shock HFinGeneral
Pulses LsoPunoedema
Bounding pulses high cardiac output (sepsis)
Weak or small pulse low cardiac output
Pulse pressure Public Domain

Systolic diastolic pressure

High = high cardiac output
Low = low cardiac output
Obstructive Shock
Obstruction to blood flow from heart
Low cardiac output despite normal contractility
Large Pericardial Effusion
Tamponade
Tension pneumothorax
Massive pulmonary embolism
Low cardiac output
High SVR
Heart
Problem filling
andget blood out
heart
from
Treatment of Shock
Cardiogenic: inotropes no IV fluids
Milrinone, dobutamine
Hypovolemic: volume
Blood transfusions, IV fluids
Distributive: volume and vasopressors
Phenylephrine, epinephrine, norepinephrine
Obstructive: resolve obstruction
Treat tamponade, embolism, tension pneumothorax

by draining t chest tube

pericardial
effusion
Adrenergic Vasopressors and Inotropes
Hemodynamic Effects

1: heart rate/contractility
2: vasodilation
 Adrenergic Vasopressors and Inotropes
Alpha Beta-1 Beta-2
Drug Uses

Phenylephrine +++++ Septic shock, especially if tachycardic

Norepinephrine +++++ +++ ++ Septic shock
Epinephrine +++++ ++++ +++ Anaphylaxis
prayofchaise
Dopamine +++ ++++ ++ Cardiogenic shock
Dobutamine ++++ ++ Cardiogenic shock
Epinephrine
Dose dependent effects
Low dose: beta-1 and beta-2 agonist cardiogenic shock
Increased heart rate/contractility
Vasodilation
High dose: alpha-agonist
Vasoconstriction 2
anaphylaxis

Epinephrine
Dopamine
e
Does not cross blood brain barrier (no CNS effects)
Peripheral effects highly dependent on dose
Low dose: dopamine agonist
Vasodilation in kidney vessels
Medium dose: beta-1 agonist
Increased heart rate and contractility
High dose: alpha-agonist
Vasoconstriction

we give reedin Dopamine

dose fo
cardogenic shock
Dobutamine A
excellent for

3
cardiogenic shock

MAP pressure usually falls

TPR ( 2)
Myocyte effect > SA node
More inotropy than chronotropy

Dobutamine
Vasopressin
Used in septic shock
V1 receptor agonist
Vasoconstrictor
Milrinone Trickstone titrate carefully
Used in cardiogenic shock only
Phosphodiesterase 3 inhibitor
Increase cAMP in myocytes and vascular smooth muscle
Increased contractility
Systemic vasodilation
Arteriolar vasodilation decreased SVR
Sepsis and ARDS
Jason Ryan, MD, MPH