Download MBBS Surgery Presentations 51 Shock And Bleeding Lecture Notes

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Shock and Bleeding

1

A 35-year-old man is admitted with systolic blood pressure (BP)

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of 60 mm Hg and a heart rate (HR) of 150 bpm following a

gunshot wound to the liver . What is the effect on the kidneys?

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(A) They tolerate satisfactorily ischemia of 3?4 hours duration.
(B) They undergo further ischemia if hypothermia is present.
(C) They can become damaged, even though urine output

exceeds 1500 mL/d.

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(D) They are affected and cause an increased creatinine

clearance.

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(E) They are prevented from further damage by a vasopressor.

2

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Immediate management of a patient with Multiple

fracture and fluid loss includes the infusion -

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Blood
Dextran
Normal saline
Ringer lactate

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3

Hypotension

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In Adults:

systolic BP 90 mm Hg

mean arterial pressure 60 mm Hg

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systolic BP > 40 mm Hg from the patient's

baseline pressure

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SHOCK

Inadequate perfusion (blood flow)

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leading to inadequate oxygen delivery to

tissues

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5

"Hypoperfusion can be

present in the absence of

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significant hypotension."

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Physiology

Basic unit of life = cell
Cells get energy needed to stay alive by reacting

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oxygen with fuel (usually glucose)

No oxygen, no energy
No energy, no life

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7

Cardiovascular System

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Transports oxygen, fuel to cells
Removes carbon dioxide, waste products for

elimination from body

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Cardiovascular system must be able to

maintain sufficient flow through

capillary beds to meet cell's oxygen and

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fuel needs

8

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Flow = Perfusion

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Adequate Flow =

Inadequate Flow =

Adequate Perfusion

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Indequate Perfusion

(Hypoperfusion)

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Hypoperfusion =

Shock

9

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What is needed to maintain perfusion?

Pump

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Heart

Pipes

Blood Vessels

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Fluid

Blood

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10

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How can perfusion fail?

Pump Failure

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Pipe Failure
Loss of Volume

11

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Types of Shock and Their

Causes

12

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Cardiogenic Shock

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Pump failure
Heart's output depends on

How often it beats (heart rate)

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How hard it beats (contractility)

Rate or contractility problems cause pump failure

13

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Cardiogenic Shock

Causes

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Acute myocardial infarction
Very low heart rates (bradycardias)
Very high heart rates (tachycardias)

Why would a high heart rate caused decreased output?

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Hint: Think about when the heart fills.

14

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Neurogenic Shock

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Loss of peripheral resistance
Spinal cord injured
Vessels below injury dilate

What happens to the pressure in a

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closed system if you increase its size?

15

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Hypovolemic Shock

Loss of volume
Causes

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Blood loss: trauma
Plasma loss: burns
Water loss: Vomiting, diarrhea, sweating, increased

urine, increased respiratory loss

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If a system that is supposed to be closed

leaks, what happens to the pressure in it?

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16

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Psychogenic Shock

Simple fainting (syncope)
Caused by stress, pain, fright
Heart rate slows, vessels dilate

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Brain becomes hypoperfused
Loss of consciousness occurs

What two problems combine to produce

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hypoperfusion in psychogenic shock?

17

Septic Shock

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Results from body's response to bacteria in

bloodstream

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Vessels dilate, become "leaky"

What two problems combine to produce

hypoperfusion in septic shock?

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18

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Anaphylactic Shock

Results from severe allergic reaction
Body responds to allergen by releasing histamine

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Histamine causes vessels to dilate and become

"leaky"

What two problems combine to produce

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hypoperfusion in anaphylaxis?

19

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OBSTRUCTIVE SHOCK

Flow of blood is obstructed.

Cardiac tamponade

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Constrictive pericarditis
Tension pneumothorax.
Massive pulmonary embolism
Aortic stenosis.

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20

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PATHOPHYSIOLOGY OF

SHOCK SYNDROME

Cells switch from aerobic to anaerobic metabolism

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lactic acid production

Cell function ceases & swells

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membrane becomes more permeable

electrolytes & fluids seep in & out of cell

Na+/K+ pump impaired

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mitochondria damage

cell death

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COMPENSATORY MECHANISMS: Sympathetic

Nervous System (SNS)-Adrenal Response

Stimulated by baroreceptors

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+Increased heart rate

+Increased contractility

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+Vasoconstriction (SVR-Afterload)

+Increased Preload

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COMPENSATORY MECHANISMS:

Sympathetic Nervous System (SNS)-Adrenal

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Response

SNS - Hormonal: Renin-angiotension system

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+Decrease renal perfusion

+Releases renin

angiotension I

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+angiotension II

potent vasoconstriction &

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+releases aldosterone adrenal cortex

+sodium & water retention

COMPENSATORY MECHANISMS:

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Sympathetic Nervous System (SNS)-Adrenal

Response

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SNS - Hormonal: Antidiuretic Hormone
+Osmoreceptors in hypothalamus stimulated
+ADH released by Posterior pituitary gland

+Vasopressor effect to increase BP

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+Acts on renal tubules to retain water

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COMPENSATORY MECHANISMS:

Sympathetic Nervous System (SNS)-Adrenal

Response

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SNS - Hormonal: Adrenal Cortex
+Anterior pituitary releases adrenocorticotropic

hormone (ACTH)

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+Stimulates adrenal Cx to release glucorticoids
+Blood sugar increases to meet increased metabolic

needs

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Stages of Shock

?Initial stage - tissues are under perfused, decreased CO,

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increased anaerobic metabolism, lactic acid is building

?Compensatory stage - Reversible. SNS activated by low CO,

attempting to compensate for the decrease tissue perfusion.

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?Progressive stage - Failing compensatory mechanisms:

profound vasoconstriction from the SNS

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ISCHEMIA

Lactic acid production is high

metabolic acidosis

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?Irreversible or refractory stage - Cellular necrosis and Multiple

Organ Dysfunction Syndrome may occur

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DEATH IS IMMINENT!!!!

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Net results of cellular shock:

?systemic lactic acidosis
?decreased myocardial contractility
?decreased vascular tone

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?decrease blood pressure, preload, and

cardiac output

Case 1

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24 year old male
Previously healthy
Lives in a malaria endemic area (PNG)
Brought in by friends after a fight - he was kicked in

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the abdomen

He is agitated, and won't lie flat on the stretcher
HR 92, BP 126/72, SaO2 95%, RR 26

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Stages of Shock

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Insult

Preshock

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(Com

pe

nsa ti

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on)

Timeline and progression will

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Shockdepend

(Com

pe

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nsat i

on -Cause

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Ove

rwhel

m e

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d) -Patient Characteristics

-Intervention

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End organ

Damage

Death

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Case 1: Stages of Shock

Stage

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Pathophysiology

Clinical Findings

Insult

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Splenic Rupture -- Blood Loss Abdominal tenderness and girth

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Case 1: Stages of Shock

Stage

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Pathophysiology

Clinical Findings

Insult

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Splenic Rupture -- Blood Loss Abdominal tenderness and

girth

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Preshock Hemostatic compensation

MAP is maintained

MAP =CO(HR xSV) xSVR

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HR wil be increased

Decreased CO is compensated by Extremities wil be cool due

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increase in HR and SVR

to vasoconstriction

Case 1: Stages of Shock

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Stage

Pathophysiology

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Clinical Findings

Insult

Splenic Rupture -- Blood

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Abdominal tenderness and

Loss

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girth

Preshock

Hemostatic compensation MAP is maintained

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MAP =CO(HR xSV) x SVR HR wil be increased

Decreased CO is compensated Extremities wil be cool due to

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by increase in HR and SVR

vasoconstriction

Shock

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Compensatory mechanisms MAP is reduced

fail

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Tachycardia, dyspnea,

restlessness

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S Ca

tage se

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P 1

ath:

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o

pS

hyt

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sia

ol g

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og e

y s of Shoc

Clinical k

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Findings

Insult

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Splenic Rupture -- Blood Loss Abdominal tenderness and girth

Preshock Hemostatic compensation

MAP is maintained

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MAP =CO(HR xSV) x SVR

HR wil be increased

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Decreased CO is compensated

Extremities wil be cool due to

by increase in HR and SVR

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vasoconstriction

Shock

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Compensatory mechanisms

MAP is reduced

fail

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Tachycardia, dyspnea,

restlessness

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End

Cel death and organ failure

Decreased renal function

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organ

Liver failure

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dysfuncti

Disseminated Intravascular

on

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Coagulopathy

Death

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Si

Igns this Shock?

s

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a
n
d

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s
y
m

p

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t
o
m

s

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L

a
b

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o
r
a
t
o

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r
y

f
i

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n
d
i
n
g

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s

H

e

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m

o
d
y

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n
a
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i

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c

m

e

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a
s
u
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e

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s

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Symptoms and Signs of Shock

Level of consciousness

Initially may show few symptoms

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Continuum starts with

Anxiety

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Agitation

Confusion and Delirium

Obtundation and Coma

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In infants

Poor tone
Unfocused gaze

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Weak cry
Lethargy/Coma
(Sunken or bulging fontanelle)

Symptoms and Signs of Shock

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Pulse

Tachycardia HR > 100 - What are a few exceptions?
Rapid, weak, thready distal pulses

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Respirations

Tachypnea
Shallow, irregular, labored

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Symptoms and Signs of Shock

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Blood Pressure

May be normal!
Definition of hypotension

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Systolic < 90 mmHg

MAP < 65 mmHg

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40 mmHg drop systolic BP from from baseline

Children

Systolic BP < 1 month = < 60 mmHg

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Systolic BP 1 month - 10 years = < 70 mmHg + (2 x age in years)

In children hypotension develops late, late, late

A pre-terminal event

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Symptoms and Signs of Shock

Skin

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Cold, clammy (Cardiogenic, Obstructive, Hemorrhagic)
Warm (Distributive shock)
Mottled appearance in children
Look for petechia

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Dry Mucous membranes
Low urine output <0.5 ml/kg/hr

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Empiric Criteria for Shock

4 out of 6 criteria have to be met

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Ill appearance or altered mental status
Heart rate >100
Respiratory rate > 22 (or PaCO2 < 32 mmHg)
Urine output < 0.5 ml/kg/hr
Arterial hypotension > 20 minutes duration

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Lactate > 4

Management of Shock

History

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Physical exam
Labs
Other investigations
Treat the Shock - Start treatment as soon as you

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suspect Pre-shock or Shock

Monitor

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Historical Features

Trauma?

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Pregnant?
Acute abdominal pain?
Vomiting or Diarrhea?
Hematochezia or hematemesis?
Fever? Focus of infection?

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Chest pain?

Physical Exam

Vitals - HR, BP, Temperature, Respiratory rate,

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Oxygen Saturation

Capillary blood sugar
Weight in children

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Physical Exam

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In a patient with normal level of consciousness -

Physical exam can be directed by the history

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Physical Exam

In a patient with abnormal level of consciousness

Primary survey

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Cardiovascular (murmers, JVP, muffled heart sounds)

Respiratory exam (crackles, wheezes),

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Abdominal exam

Rectal and vaginal exam

Skin and mucous membranes

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Neurologic examination

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Laboratory Tests

CBC, Electrolytes, Creatinine/BUN, glucose
+/- Lactate

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+/- Capillary blood sugar
+/- Cardiac Enzymes
Blood Cultures
Beta HCG
+/- Cross Match

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Other investigations

ECG
Urinalysis

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CXR
+/- Echo
+/- FAST

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Treatment

Start treatment immediately

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Stages of Shock

Insult

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Preshock

(Com

pe

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nsa ti

on)

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Early Intervention can arrest or


Shoc k reduce the damage

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(Compensation

Overwhelmed)

End organ

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Damage

Death

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Treatment

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ABC's "5 to 15"

Airway
Breathing
Circulation

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Put the patient on a monitor if available

Treat underlying cause

Treatment: Airway and

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Breathing

Give oxygen

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Treatment: Airway and Breathing

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Consider Intubation

Is the cause quickly reversible?

Generally no need for intubation

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3 reasons to intubate in the setting of shock

Inability to oxygenate

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Inability to maintain airway

Work of breathing

Treatment: Circulation

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Treat the early signs of shock (Cold, clammy?

Decreased capillary refill? Tachycardic? Agitated?)

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DO NOT WAIT for hypotension

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Treatment: Circulation

Start IV +/- Central line (or Intraosseous)
Do Blood Work +/- Blood Cultures

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Treatment: Circulation

Fluids - 20 ml/kg bolus x 3

Normal saline

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Ringer's lactate

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Back to Case 1

24 year old male
Previously healthy
Lives in a malaria endemic area (PNG)

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Brought in by friends after a fight - he was kicked in

the abdomen

He is agitated, and won't lie flat on the stretcher

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HR 92, BP 126/72, SaO2 95%, RR 26

Case 1

On examination

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Extremely agitated
Clammy and cold
Heart exam - normal
Chest exam - good air entry

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Abdomen - bruised, tender, distended
No other signs of trauma

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Case 1: Management

Hemorrhagic (Hypovolemic Shock)

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ABC's

Monitors

O2

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Intubate?

IV lines x 2, Fluid boluses, Call for Blood - O type

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Blood work including cross match

Treat Underlying Cause

Case 1: Management

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Hemorrhagic (Hypovolemic Shock)

ABC's

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Monitors

O2

Intubate?

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IV lines x 2, Fluid boluses, Call for Blood - O type

Blood work including cross match

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Treat Underlying Cause

Give Blood

Call the surgeon stat

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If the patient does not respond to initial boluses and blood products

- take to the Operating Room

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Blood Products

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Use blood products if no improvement to fluids

PRBC 5-10 ml/kg

O- in child-bearing years and O+ in everyone else

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+/- Platelets

Case 2

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23 year old woman
Has been fatigued and short of breath for a few days
She fainted and family brought her in
They tell you she has a heart problem

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Case 2

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HR 132, BP 76/36, SaO2 88%, RR 30, Temp 36.3
Appearance - obtunded
Cardiovascular exam - S1, S2, irregular, holosytolic

murmer, JVP is 5 cm , no edema

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Chest - bilateral crackles, accessory muscle use
Abdomen - unremarkable
Rest of exam is normal

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Stages of Shock

Insult

Preshock

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(Compensation)

What stage is she at?

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Shock

(Com pe

nsat i

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on

Overwhelmed)

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End organ

Damage

Death

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Case 2: Management

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Cardiogenic Shock

ABC's

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Monitors

O2

IV and blood work

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ECG - Atrial Fibrillation, rate 130's

Treat Underlying Cause

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Case 2: Management

Cardiogenic Shock

ABC's

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Monitors

O2

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IV and blood work

Intubate?

ECG - Atrial Fibrillation, rate 130's

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Treat Underlying Cause

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Case 2: Why would you

intubate?

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Is the cause quickly reversible?

UNLIKELY

3 reasons to intubate in the setting of shock

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Inability to oxygenate

Inability to oxygenate

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Inability to maintain airway

(Pulmonary edema,

SaO2 88%)

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Work of breathing

Accessory

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Muscle Use

Case 2: Why Intubate?

Strenuous use of accessory respiratory muscles (i.e.

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work of breathing) can:

Increase O2 consumption by 50-100%
Decrease cerebral blood flow by 50%

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Case 2: Management

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Cardiogenic Shock

ABC's

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Monitors

O2

IV and blood work

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Intubate?

ECG - Atrial Fibrillation, rate 130's

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Treat Underlying Cause

Case 2: Management

Cardiogenic Shock

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Treat Underlying Cause

Lasix

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Atrial Fibrillation - Cardioversion? Rate control?

Inotropes - Dobutamine +/- Norepinephrine (Vasopressor)

Look for precipitating causes - infectious?

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Vasopressors in Cardiogenic

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Shock

Norepinephrine
Dopamine

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Epinephrine
Phenylephrine

Case 3

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36 year old woman
Pedestrian hit by a car
She is brought into the hospital 2 hrs after accident
Short of breath
Has been complaining of chest pain

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Case 3

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HR 126, SBP 82, SaO2 70%, RR 36, Temp 35
Obtunded, Accessory muscle use
Trachea is deviated to Left
Heart - distant heart sounds

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Chest - decreased air entry on the right, broken ribs,

subcutaneous emphysema

Abdominal exam - normal

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Apart from bruises and scrapes no other signs of

trauma

Stages of Shock

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Insult

Preshock

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(Compensation)

What stage is she at?

Shock

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(Com pe

nsat i

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on

Overwhelmed)

End organ

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Damage

Death

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Case 3: Management

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Obstructive Shock

ABC's

Monitors

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O2

IV

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Intubate?

BW

Treat Underlying Cause

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Case 3: Management

Obstructive Shock

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ABC's

Monitors

O2

--- Content provided by​ FirstRanker.com ---

IV

Intubate?

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BW

Treat Underlying Cause

Needle thoracentesis

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Chest tube

CXR

--- Content provided by FirstRanker.com ---

Case 3: Management

--- Content provided by‍ FirstRanker.com ---

Obstructive Shock

ABC's

Monitors

--- Content provided by‍ FirstRanker.com ---

O2

IV

--- Content provided by⁠ FirstRanker.com ---

Intubate?

BW

Treat Underlying Cause

--- Content provided by‌ FirstRanker.com ---

Needle thoracentesis

Chest tube

--- Content provided by​ FirstRanker.com ---

CXR

Case 3: Management

Obstructive Shock

--- Content provided by FirstRanker.com ---

ABC's

Monitors

--- Content provided by​ FirstRanker.com ---

O2

IV

Intubate?

--- Content provided by⁠ FirstRanker.com ---

BW

Treat Underlying Cause

--- Content provided by FirstRanker.com ---

Needle thoracentesis

Chest tube

CXR

--- Content provided by‍ FirstRanker.com ---

Intubate if no response

--- Content provided by​ FirstRanker.com ---

Case 3

You perform a needle thoracentesis - hear a hissing

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sound

Chest tube is inserted successfully
HR 96, BP 100/76, SaO2 96% on O2, RR 26
You resume your clinical duties, and call the surgeon

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Case 3

1 hr has gone by
You are having lunch

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The nurse puts her head through the door to tell you

about another patient at triage, and as she is leaving

"By the way, that woman with the chest tube, is

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feeling not so good" and leaves.

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Case 3

You are back at the bedside
The patient is obtunded again

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Pale and Clammy
HR 130, BP 86/52, SaO2 96% on O2
Chest tube seems to be working
Trachea is midline
Heart - Normal

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Chest - Good air entry
Abdomen - decreased bowel sounds, distended

Combined Shock

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Different types of shock can coexist
Can you think of other examples?

--- Content provided by FirstRanker.com ---

Monitoring

Vitals - BP, HR, SaO2
Mental Status

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Urine Output (> 1-2 ml/kg/hr)
When something changes or if you do not observe a

response to your treatment -

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re-examine the patient

Can we measure cel hypoxia?

Lactate - we already talked about - a surrogate

--- Content provided by‌ FirstRanker.com ---

Venous Oxygen Saturation - more direct measure

--- Content provided by‌ FirstRanker.com ---

Venous Oxygen Saturation

Hg carries O2

--- Content provided by‍ FirstRanker.com ---

A percentage of O2 is extracted by the tissue for

cellular respiration

Usually the cells extract < 30% of the O2

--- Content provided by‌ FirstRanker.com ---

Venous Oxygen Saturation

Svo2 = Mixed venous oxygen saturation

--- Content provided by FirstRanker.com ---

Measured from pulmonary artery by Swan-Ganz catheter.

v Normal > 65%

Scvo2 = Central venous oxygen saturation

--- Content provided by‌ FirstRanker.com ---

Measured through central venous cannulation of SVC or R Atrium

- i.e. Central Line

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v Normal > 70%

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PART 2

Case 4

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40 year old male
RUQ abdominal pain, fever, fatigued for 5-6 days
No past medical history

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Case 4

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HR 110, BP 100/72, SaO2 96%, T 39.2, RR 26
Drowsy
Warm skin
Heart - S1, S2, no Murmers
Chest - good A/E x 2

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Abdomen - decreased bowel sound, tender RUQ

Stages of Shock

Insult

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Preshock

(Compensation)

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What stage is he at?

Shock

(Com pe

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nsat i

on

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Overwhelmed)

End organ

Damage

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Death

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Stages of Sepsis

SIRS

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SEPSIS

SEVERE

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SE

PSIS

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SEPTIC

SHOCK

MODS/DEATH

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Definitions of Sepsis

Systemic Inflammatory Response Syndrome (SIRS) ? 2

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or > of:

-Temp > 38 or < 36

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-RR > 20
-HR > 90/min

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-WBC >12,000 or <6,000 or more than 10%
immature bands

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Definitions of Sepsis

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Sepsis ? SIRS with proven or suspected

microbial source

--- Content provided by‌ FirstRanker.com ---

Severe Sepsis ? sepsis with one or more signs of

organ dysfunction or hypoperfusion.

Definitions of Sepsis

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Septic shock = Sepsis + Refractory

hypotension
-Unresponsive to initial fluids 20-40cc/kg ?

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Vasopressor dependant

MODS ? multiple organ dysfunction

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syndrome
-2 or more organs

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Stages of Sepsis

Mortality

--- Content provided by FirstRanker.com ---

SIRS

7%

SEPSIS

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16%

SEVERE

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20%



SE

--- Content provided by‌ FirstRanker.com ---

PSIS

SEPTIC

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70%

SHOCK

MODS/DEATH

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Pathophysiology

Complex pathophysiologic mechanisms

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Pathophysiology

--- Content provided by⁠ FirstRanker.com ---

Inflammatory Cascade:

Humoral, cellular and Neuroendocrine (TNF, IL etc)

Endothelial reaction

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Endothelial permeability = leaking vessels

Coagulation and complement systems

--- Content provided by FirstRanker.com ---

Microvascular flow impairment

Pathophysiology

End result = Global Cellular Hypoxia

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Focus of Infection

--- Content provided by⁠ FirstRanker.com ---

Any focus of infection can cause sepsis

Gastrointestinal
GU

--- Content provided by‍ FirstRanker.com ---

Oral
Skin

Risk Factors for Sepsis

--- Content provided by​ FirstRanker.com ---

Infants
Immunocompromised patients

Diabetes
Steroids

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HIV
Chemotherapy/malignancy
Malnutrition

Sickle cell disease

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Disrupted barriers

Foley, burns, central lines, procedures

--- Content provided by​ FirstRanker.com ---

Back to Case 4

HR 110, BP 100/72, SaO2 96%, T 39.2, RR 20

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Drowsy
Warm skin
Heart - S1, S2, no Murmers
Chest - good A/E x 2
Abdomen - decreased bowel sound, tender RUQ

--- Content provided by‌ FirstRanker.com ---

Case 4: Management

Distributive Shock (SEPSIS)

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ABC's

Monitors

O2

--- Content provided by​ FirstRanker.com ---

IV fluids 20 cc/kg x 3

Intubate?

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BW

Treat Underlying Cause

--- Content provided by‍ FirstRanker.com ---

Resuscitation in Sepsis

Early goal directed therapy - Rivers et al NEJM 2001

--- Content provided by‌ FirstRanker.com ---

Used in pt's who have: an infection, 2 or more SIRS, have a

systolic < 90 after 20-30cc/ml or have a lactate > 4.

--- Content provided by​ FirstRanker.com ---

Emergency patients by emergency doctors

Resuscitation protocol started early - 6 hrs

Resuscitation in Sepsis: EGDT

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The theory is to normalize...

Preload - 1st
Afterload - 2nd

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Contractility - 3rd

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BACK TO OUR EQUATION

MAP = CO x SVR

--- Content provided by FirstRanker.com ---

(HR x Stroke volume)

Preload

--- Content provided by​ FirstRanker.com ---

Afterload

Contractility

BACK TO OUR EQUATION

--- Content provided by‌ FirstRanker.com ---

MAP = CO x SVR

(HR x Stroke volume)

--- Content provided by‌ FirstRanker.com ---

Preload

Afterload

Contractility

--- Content provided by‍ FirstRanker.com ---

Preload

--- Content provided by‍ FirstRanker.com ---

Dependent on intravascular volume

If depleted intravascular volume (due to increased endothelial

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permeability) - PRELOAD DECREASES

Can use the CVP as measurement of preload

Normal = 8-12 mm Hg

--- Content provided by FirstRanker.com ---

Preload

How do you correct decreased preload (or intravascular volume)

--- Content provided by‌ FirstRanker.com ---

Give fluids
Rivers showed an average of 5 L in first 6 hours

What is the end point?

--- Content provided by​ FirstRanker.com ---

BACK TO OUR EQUATION

--- Content provided by​ FirstRanker.com ---

MAP = CO x SVR

(HR x Stroke volume)

Preload

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Afterload

Contractility

--- Content provided by FirstRanker.com ---

Afterload

Afterload determines tissue perfusion

Using the MAP as a surrogate measure - Keep between 60-90 mm

--- Content provided by⁠ FirstRanker.com ---

Hg

In sepsis afterload is decreased d/t loss of vessel tone

--- Content provided by‍ FirstRanker.com ---

Afterload

--- Content provided by‌ FirstRanker.com ---

How do you correct decreased afterload?

Use vasopressor agent

Norepinephrine

--- Content provided by​ FirstRanker.com ---

Alternative Dopamine or Phenylpehrine

BACK TO OUR EQUATION

MAP = CO x SVR

--- Content provided by⁠ FirstRanker.com ---

(HR x Stroke volume)

Preload

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Afterload

Contractility

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Contractility

Use the central venous oxygen saturation (ScvO2)

--- Content provided by⁠ FirstRanker.com ---

as a surrogate measure

Shown to a be a surrogate for cardiac index

--- Content provided by⁠ FirstRanker.com ---

Keep > 70%

Contractility

How to improve ScvO2 > 70%?

--- Content provided by⁠ FirstRanker.com ---

Optimize arterial O2 with non-rebreather

Ensure a hematocrit > 30 (Transfuse to reach a hematocrit of > 30)

--- Content provided by⁠ FirstRanker.com ---

Use Inotrope - Dobutamine 2.5ug/kg per minute and titrated (max 20ug/kg)

Respiratory Support - Intubation (Don't forget to sedate and paralyze)

--- Content provided by‍ FirstRanker.com ---

Suspect infection

EGDT

--- Content provided by‍ FirstRanker.com ---

Document source within 2hrs

The high risk pt: Systolic < 90 after bolus

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Or

Lactate > 4mmol/l

Abx within 1 hr

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+ source control

<8mm hg

--- Content provided by​ FirstRanker.com ---

CVP

Crystalloid

Decrease 02

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> 8 ?12 mm hg

Consumption

--- Content provided by​ FirstRanker.com ---

<65 or >90mmhg

MAP

Vasoactive

--- Content provided by FirstRanker.com ---

INTUBATE

agent

--- Content provided by⁠ FirstRanker.com ---

> 65 ? 95mm hg

<70%

Scv02

--- Content provided by⁠ FirstRanker.com ---

Packed RBC

to Hct >30%

--- Content provided by‍ FirstRanker.com ---

>70%

<70%

>70%

--- Content provided by FirstRanker.com ---

Inotropes

NO

--- Content provided by​ FirstRanker.com ---

Goals Achieved

Suspect infection

EGDT

--- Content provided by‌ FirstRanker.com ---

Document source within 2hrs

The high risk pt: systolic < 90 after bolus

--- Content provided by FirstRanker.com ---

Or

INTUBATE

Lactate > 4mmol/l

--- Content provided by⁠ FirstRanker.com ---

EARLY

IF IMPENDING

--- Content provided by‍ FirstRanker.com ---

Abx within 1 hr

RESPIRATORY

FAILURE

--- Content provided by‌ FirstRanker.com ---

+ source control

<8mm hg

--- Content provided by‌ FirstRanker.com ---

CVP

Crystalloid

Decrease 02

--- Content provided by‍ FirstRanker.com ---

> 8 ?12 mm hg

Consumption

--- Content provided by FirstRanker.com ---

<65 or >90mmhg

MAP

Vasopressor

--- Content provided by‌ FirstRanker.com ---

INTUBATE

> 65 ? 95mm hg

--- Content provided by‍ FirstRanker.com ---

<70%

Scv02

Packed RBC

--- Content provided by⁠ FirstRanker.com ---

to Hct >30%

>70%

--- Content provided by‌ FirstRanker.com ---

<70%

>70%

Inotropes

--- Content provided by​ FirstRanker.com ---

NO

Goals Achieved

--- Content provided by FirstRanker.com ---

Suspect infection

--- Content provided by‍ FirstRanker.com ---

MODIFIED

Document source within 2hrs

The high risk pt: systolic < 90 after bolus

--- Content provided by⁠ FirstRanker.com ---

INTUBATE EARLY

IF IMPENDING

--- Content provided by⁠ FirstRanker.com ---

RESPIRATORY

Abx within 1 hr

FAILURE

--- Content provided by​ FirstRanker.com ---

And source control

< 65 mmHg

--- Content provided by​ FirstRanker.com ---

MAP (Urine

More fluids

Decrease 02

--- Content provided by‌ FirstRanker.com ---

>65 mmHgOutput)

Consumption

--- Content provided by‍ FirstRanker.com ---

<65 mmHg

MAP

Vasopressors

--- Content provided by​ FirstRanker.com ---

INTUBATE

>65mm hg

--- Content provided by‍ FirstRanker.com ---

< 10 %

Lactate

Packed RBC

--- Content provided by‌ FirstRanker.com ---

Clearance

to Hct >30%

--- Content provided by⁠ FirstRanker.com ---

> 10%

< 10%

> 10%

--- Content provided by⁠ FirstRanker.com ---

Inotropes

NO

--- Content provided by⁠ FirstRanker.com ---

Goals Achieved

Case 4: Management

Distributive Shock (SEPSIS)

--- Content provided by​ FirstRanker.com ---

ABC's

Monitors

--- Content provided by‌ FirstRanker.com ---

O2

IV fluids 20 cc/kg

Intubate

--- Content provided by‍ FirstRanker.com ---

BW

Treat Underlying Cause

--- Content provided by‌ FirstRanker.com ---

Acetaminophen

Antibiotics - GIVE EARLY

Source control - the 4 D's = Drain, Debride, Device removal,

--- Content provided by‍ FirstRanker.com ---

Definitive Control

--- Content provided by​ FirstRanker.com ---

Antibiotics

Early Antibiotics

--- Content provided by FirstRanker.com ---

Within 3-6hrs can reduce mortality - 30%

Within 1 hr for those severely sick

--- Content provided by⁠ FirstRanker.com ---

Don't wait for the cultures ? treat empirically then

change if need.

--- Content provided by⁠ FirstRanker.com ---

Other treatments for severe

sepsis:

Glucocorticoids

--- Content provided by FirstRanker.com ---

Glycemic Control
Activated protein C

--- Content provided by FirstRanker.com ---

Couple of words about Steroids

in sepsis...

--- Content provided by​ FirstRanker.com ---

New Guidelines for the management of sepsis

and septic shock = Surviving Sepsis Campaign

--- Content provided by‍ FirstRanker.com ---

Grade 2C ? consider steroids for septic shock in patients

with BP that responds poorly to fluid resuscitation and

vasopressors

--- Content provided by‌ FirstRanker.com ---

Critical Care Med 2008 Jan 36:296

Concluding Remarks

--- Content provided by⁠ FirstRanker.com ---

Know how to distinguish different types of shock and

treat accordingly

Look for early signs of shock

--- Content provided by‌ FirstRanker.com ---

SHOCK = hypotension

--- Content provided by⁠ FirstRanker.com ---

Concluding Remarks

Choose cost effective and high impact interventions

--- Content provided by‌ FirstRanker.com ---

Do not need central lines and ScvO2

measurements to make an impact!!

Concluding Remarks

--- Content provided by​ FirstRanker.com ---

ABC's "5 to 15"

Can't intubate?

--- Content provided by⁠ FirstRanker.com ---

Give oxygen

Develop algorithms for bag valve mask ventilation

Treat fever to decrease respiratory rate

--- Content provided by‌ FirstRanker.com ---

Treat early with fluids - need lots of it!!

--- Content provided by FirstRanker.com ---

Concluding Remarks

Monitor the patient

--- Content provided by‍ FirstRanker.com ---

Do not need central venous pressure and ScvO2
Use the HR, MAP, mental status, urine output
Lactate clearance?

Concluding Remarks

--- Content provided by‍ FirstRanker.com ---

Start antibiotics within an hour!

Do not wait for cultures or blood work

--- Content provided by‍ FirstRanker.com ---

A 22 year old man was driving drunk and without his seatbelt fastened when

--- Content provided by​ FirstRanker.com ---

he was involved in a

single-vehicle automobile accident. When attended by EMT personnel, no

information was

--- Content provided by‍ FirstRanker.com ---

available about the time of the accident. He was found agitated and

complaining of abdominal

--- Content provided by‌ FirstRanker.com ---

pain. His airway was patent. At the scene, he was breathing at 20 per minute

with a blood

pressure of 90/60 and a pulse of 130. He was placed in a hard cervical collar

--- Content provided by‌ FirstRanker.com ---

and on a back board

and transported to your emergency room. Upon arrival his vital signs are the

--- Content provided by‌ FirstRanker.com ---

same, with a

temperature of 36oC. His abdomen is markedly distended. His hands and feet

are cold, his legs

--- Content provided by‍ FirstRanker.com ---

mottled. A nasogastric tube reveals green liquid. A urinary catheter reveals

dark yellow urine. His

--- Content provided by⁠ FirstRanker.com ---

hemoglobin is 7. His abdominal lavage reveals gross blood.

135

Study Questions:

--- Content provided by‍ FirstRanker.com ---

What type of shock does this patient exhibit?
What would be the cardiac output (low, normal,

high)?

--- Content provided by‍ FirstRanker.com ---

What would be the systematic resistance (low,

normal, high)?

What would be the central venous and/or pulmonary

--- Content provided by⁠ FirstRanker.com ---

capillary occlusion pressure (low, normal,

high)?
What therapy would reverse the shock?

--- Content provided by‍ FirstRanker.com ---

136

--- Content provided by FirstRanker.com ---

A 65 year old man with known coronary artery disease

(myocardial infarct three years earlier,

--- Content provided by‌ FirstRanker.com ---

currently taking a beta blocker) is admitted with acute

left lower quadrant pain of six hours duration.

His blood pressure is 90/50, pulse 120, respirations 18,

--- Content provided by⁠ FirstRanker.com ---

temperature 39oC. He is flushed with

warm hands and warm feet, his legs are pink. Physical

--- Content provided by FirstRanker.com ---

examination reveals findings consistent

with peritonitis in the left lower quadrant.

137

--- Content provided by FirstRanker.com ---

Study Questions:
What type of shock does this patient exhibit?
What would be the cardiac output (low, normal,

--- Content provided by​ FirstRanker.com ---

high)?

What would be the systemic resistance (low, normal,

high)?

--- Content provided by⁠ FirstRanker.com ---

What would be the central venous and/or pulmonary

capillary occlusion pressure (low, normal,

--- Content provided by‌ FirstRanker.com ---

high)?
What therapy would reverse the shock?

138

--- Content provided by‌ FirstRanker.com ---

A 35 year old man dove into three feet of water at a

--- Content provided by⁠ FirstRanker.com ---

swimming pool, did not emerge and was

rescued by friends who performed CPR. When the EMTs

arrived they found the patient to have a

--- Content provided by‌ FirstRanker.com ---

blood pressure of 80/50, pulse 100, and no spontaneous

respirations, although he was opening his

--- Content provided by‍ FirstRanker.com ---

eyes. They began ambu bag assistance of respiration and

placed a hard cervical collar. He was

placed on a back board and transported to your emergency

--- Content provided by‌ FirstRanker.com ---

room. Upon arrival he has the same

vital signs with warm hands and feet and pink extremities.

--- Content provided by‌ FirstRanker.com ---

139

STAGES OF SHOCK

140

--- Content provided by​ FirstRanker.com ---

--- Content provided by‌ FirstRanker.com ---

Types of Shock and Their

Causes

--- Content provided by‌ FirstRanker.com ---

141

Cardiogenic Shock

Pump failure

--- Content provided by‍ FirstRanker.com ---

Heart's output depends on

How often it beats (heart rate)
How hard it beats (contractility)

--- Content provided by​ FirstRanker.com ---

Rate or contractility problems cause pump failure

142

--- Content provided by‍ FirstRanker.com ---

Cardiogenic Shock

Causes

--- Content provided by⁠ FirstRanker.com ---

Acute myocardial infarction
Very low heart rates (bradycardias)
Very high heart rates (tachycardias)

--- Content provided by‍ FirstRanker.com ---

Why would a high heart rate caused decreased output?

Hint: Think about when the heart fills.

143

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144

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145

Neurogenic Shock

--- Content provided by‌ FirstRanker.com ---

Loss of peripheral resistance
Spinal cord injured
Vessels below injury dilate

What happens to the pressure in a

--- Content provided by‌ FirstRanker.com ---

closed system if you increase its size?

146

--- Content provided by FirstRanker.com ---

Hypovolemic Shock

--- Content provided by FirstRanker.com ---

Loss of volume
Causes

Blood loss: trauma
Plasma loss: burns

--- Content provided by FirstRanker.com ---

Water loss: Vomiting, diarrhea, sweating, increased

urine, increased respiratory loss

If a system that is supposed to be closed

--- Content provided by FirstRanker.com ---

leaks, what happens to the pressure in it?

147

--- Content provided by​ FirstRanker.com ---

148

--- Content provided by‍ FirstRanker.com ---

Psychogenic Shock

Simple fainting (syncope)
Caused by stress, pain, fright
Heart rate slows, vessels dilate

--- Content provided by‍ FirstRanker.com ---

Brain becomes hypoperfused
Loss of consciousness occurs

What two problems combine to produce

--- Content provided by⁠ FirstRanker.com ---

hypoperfusion in psychogenic shock?

149

Septic Shock

--- Content provided by‍ FirstRanker.com ---

Results from body's response to bacteria in

bloodstream

--- Content provided by‍ FirstRanker.com ---

Vessels dilate, become "leaky"

What two problems combine to produce

hypoperfusion in septic shock?

--- Content provided by FirstRanker.com ---

150

--- Content provided by​ FirstRanker.com ---

Anaphylactic Shock

Results from severe allergic reaction
Body responds to allergen by releasing histamine

--- Content provided by‍ FirstRanker.com ---

Histamine causes vessels to dilate and become

"leaky"

What two problems combine to produce

--- Content provided by​ FirstRanker.com ---

hypoperfusion in anaphylaxis?

151

--- Content provided by‍ FirstRanker.com ---

OBSTRUCTIVE SHOCK

In this situation the flow of blood is obstructed which

impedes circulation and can result in circulatory arrest.

--- Content provided by⁠ FirstRanker.com ---

Several conditions result in this form of shock.

Cardiac tamponade in which fluid in the pericardium prevents

--- Content provided by‍ FirstRanker.com ---

inflow of blood into the heart (venous return). Constrictive

pericarditis, in which the pericardium shrinks and hardens, is

similar in presentation.

--- Content provided by‍ FirstRanker.com ---

Tension pneumothorax. Through increased intrathoracic pressure,

bloodflow to the heart is prevented (venous return).

--- Content provided by⁠ FirstRanker.com ---

Massive pulmonary embolism is the result of a thromboembolic

incident in the bloodvessels of the lungs and hinders the return of

blood to the heart.

--- Content provided by FirstRanker.com ---

Aortic stenosis hinders circulation by obstructing the

ventricular outflow tract

--- Content provided by⁠ FirstRanker.com ---

152

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ENDOCRINE SHOCK

Hypothyroidism, in critically ill patients, reduces cardiac

output and can lead to hypotension and respiratory

--- Content provided by FirstRanker.com ---

insufficiency.

Thyrotoxicosis may induce a reversible cardiomyopathy.
Acute adrenal insufficiency is frequently the result of

--- Content provided by‌ FirstRanker.com ---

discontinuing corticosteroid treatment without tapering the

dosage. However, surgery and intercurrent disease in

--- Content provided by​ FirstRanker.com ---

patients on corticosteroid therapy without adjusting the

dosage to accommodate for increased requirements may also

result in this condition.

--- Content provided by‍ FirstRanker.com ---

Relative adrenal insufficiency in critically ill patients where

present hormone levels are insufficient to meet the higher

--- Content provided by‍ FirstRanker.com ---

demands .

153

Shock:

--- Content provided by‍ FirstRanker.com ---

Signs and Symptoms

Restlessness, anxiety

--- Content provided by FirstRanker.com ---

Nausea, vomiting

Increased pulse rate

Thirst

--- Content provided by‍ FirstRanker.com ---

Decreasing level of

Diminished urine output

--- Content provided by⁠ FirstRanker.com ---

consciousness

Dull eyes
Rapid, shallow respirations

--- Content provided by‌ FirstRanker.com ---

Why are these signs and symptoms present?

Hint: Think hypoperfusion

154

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155

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156

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Shock:

Signs and Symptoms

--- Content provided by‌ FirstRanker.com ---

Hypovolemia will cause

Neurogenic shock will cause:

Weak, rapid pulse

--- Content provided by FirstRanker.com ---

Weak, slow pulse

Pale, cool, clammy skin

--- Content provided by⁠ FirstRanker.com ---

Dry, flushed skin

Cardiogenic shock may cause:

Sepsis and anaphylaxis will

--- Content provided by⁠ FirstRanker.com ---

Weak, rapid pulse or weak, slow

cause:

--- Content provided by​ FirstRanker.com ---

pulse

Weak, rapid pulse

Pale, cool, clammy skin

--- Content provided by‍ FirstRanker.com ---

Dry, flushed skin

Can you explain the differences in the

--- Content provided by FirstRanker.com ---

signs and symptoms?

157

Shock: Signs and Symptoms

--- Content provided by‌ FirstRanker.com ---

Patients with anaphylaxis will:

Develop hives (urticaria)
Itch

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Develop wheezing and difficulty breathing

(bronchospasm)

What chemical released from the body during an

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allergic reaction accounts for these effects?

158

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Shock:

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Signs and Symptoms

Shock is NOT the same thing

as a low blood pressure!

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A falling blood pressure

is a LATE sign of shock!

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159

Shock:

Signs and Symptoms

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Obscure/Less viewed symptom of shock

Drop in end tidal carbon dioxide (ETCO2) level
Indicative of respiratory failure resulting in poor

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oxygenation, therefore, poor perfusion or Shock

160

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Severity of shock

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Compensated shock
body's cardiovascular and endocrine compensatory

responses reduce flow to non-essential organs to

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preserve preload and flow to the lungs and brain.

Apart from a tachycardia and cool peripheries

(vasoconstriction, circulating catecholamines) there

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may be no other clinical signs of hypovolaemia.

161

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Decompensation
Further loss of circulating volume overloads the

body's compensatory mechanisms and there is

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progressive renal, respiratory and cardiovascular

decompensation.

In general, loss of around 15% of the circulating blood

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volume is within normal compensatory mechanisms.

Blood pressure is usually well maintained and only

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falls after 30?40% of the circulating volume has been

lost.

162

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Mild shock

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Initially there is tachycardia, tachypnoea and a mild

reduction in urine output and mild anxiety.

Blood pressure is maintained although there is a

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decrease in pulse pressure.

The peripheries are cool and sweaty with prolonged

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capillary refill times (except in septic distributive

shock).

163

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Moderate shock
As shock progresses, renal compensatory mechanisms

fail, renal perfusion falls and urine output dips below

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0.5 ml kg?1h?1.

There is further tachycardia and now the blood

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pressure starts to fall.

Patients become drowsy and mildly confused.

164

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Severe shock

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In severe shock there is profound tachycardia and

hypotension.

Urine output falls to zero and patients are

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unconscious with laboured respiration

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Treatment

Secure, maintain airway (ABC's)
High concentration oxygen
Assist ventilations

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Control obvious bleeding (consider TraumaDex?)
Stabilize fractures
Replace Fluids
Prevent loss of body heat
Transport rapidly to appropriate facility

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166

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Treatment

Elevate lower extremities 8 to 12 inches in

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hypovolemic shock (Trendelenberg Position)

Do NOT elevate the lower extremities in

cardiogenic shock

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Why the difference in

management?

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167

Treatment

Administer nothing by mouth, even if the patient

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complains of thirst

168

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TREATMENT

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Immediate intervention, even before a diagnosis is

made.

Re-establishing perfusion to the organs is the primary

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goal.

Restoring and maintaining the blood circulating

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volume ensuring oxygenation and blood pressure are

adequate, achieving and maintaining effective cardiac

function, and preventing complications. )

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Intubation and mechanical ventilation may be

necessary.

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169

In hypovolemic shock, caused by bleeding, it is necessary to

immediately control the bleeding and restore the casualty's blood

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volume by giving infusions of isotonic crystalloid solutions. Blood

transfusions, packed red blood cells (RBCs), Albumin (or other colloid

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solutions), or fresh-frozen plasma are necessary for loss of large

amounts of blood (e.g. greater than 20% of blood volume), but can be

avoided in smaller and slower losses. Hypovolemia due to burns,

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diarrhea, vomiting, etc. is treated with infusions of electrolyte

solutions that balance the nature of the fluid lost. Sodium is essential

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to keep the fluid infused in the extracellular and intravascular space

whilst preventing water intoxication and brain swelling. Metabolic

acidosis (mainly due to lactic acid) accumulates as a result of poor

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delivery of oxygen to the tissues, and mirrors the severity of the shock.

It is best treated by rapidly restoring intravascular volume and

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perfusion as above. Inotropic and vasoconstrictive drugs should be

avoided, as they may interfere in knowing blood volume has returned

to normal

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170

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TREATMENT

In hypovolemic shock, caused by bleeding, it is

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necessary to immediately control the bleeding and

restore the casualty's blood volume by giving

infusions of isotonic crystalloid solutions.

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Blood transfusions, packed red blood cells (RBCs),

Albumin (or other colloid solutions), or fresh-frozen

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plasma are necessary for loss of large amounts of

blood (e.g. greater than 20% of blood volume).

Hypovolemia due to burns, diarrhea, vomiting, etc. is

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treated with infusions of electrolyte solutions that

balance the nature of the fluid lost.

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171

TREATMENT

Opinion varies on the type of fluid used in shock. The most common

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are:

Crystalloids - Such as sodium chloride (0.9%), or Lactated Ringer's.

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Dextrose solutions which contain free water are less effective at re-

establishing circulating volume, and promote hyperglycaemia.

Colloids - For example, polysaccharide (Dextran), polygeline

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(Haemaccel), succunylated gelatin (Gelofusine) and hetastarch

(Hepsan). Colloids are, in general, much more expensive than

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crystalloid solutions and have not conclusively been shown to be of

any benefit in the initial treatment of shock.

Combination - Some clinicians argue that individually, colloids and

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crystalloids can further exacerbate the problem and suggest the

combination of crystalloid and colloid solutions.

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Blood - Essential in severe hemorrhagic shock, often pre-warmed and

rapidly infused.

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TREATMENT-HAEMORRHAGIC

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SHOCK

It is to be noted that NO plain water should be given

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to the patient at any point, as the patient's low

electrolyte levels would easily cause water

intoxication, leading to premature death.

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An isotonic or solution high in electrolytes should be

administered if intravenous delivery of recommended

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fluids is unavailable.

173

TREATMENT-HAEMORRHAGIC

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SHOCK

Vasoconstrictor agents have no role in the initial

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treatment of hemorrhagic shock, due to their relative

inefficacy in the setting of acidosis.

Definitive care and control of the hemorrhage is

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absolutely necessary, and should not be delayed.

174

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TREATMENT-CARDIOGENIC

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SHOCK

In cardiogenic shock, depending on the type of

myocardal infarction, one can infuse fluids or in shock

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refractory to infusing fluids, inotropic agents.

Inotropic agents, which enhance the heart's pumping

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capabilities, are used to improve the contractility and

correct the hypotension.

Should that not suffice, an intra-aortic balloon pump

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can be considered (which reduces the workload for

the heart and improves perfusion of the coronary

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arteries) or a left ventricular assist device (which

augments the pump-function of the heart.)

175

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TREATMENT CARDIOGENIC

SHOCK

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The main goals of the treatment of cardiogenic shock

are the re-establishment of circulation to the

myocardium, minimising heart muscle damage and

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improving the heart's effectiveness as a pump.

This is most often performed by percutaneous

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coronary intervention and insertion of a stent in the

culprit coronary lesion or sometimes by cardiac

bypass.

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176

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TREATMENT

The main way to avoid the deadly consequence of

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death is to make the blood pressure rise again with:

fluid replacement with intravenous infusions
use of vasopressing drugs (e.g. to induce

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vasoconstriction);

use of anti-shock trousers that compress the legs and

concentrate the blood in the vital organs (lungs, heart,

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brain).

use of blankets to keep the patient warm - metallic

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PET film emergency blankets are used to reflect the

patient's body heat back to the patient

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TREATMENT

In distributive shock caused by sepsis the infection is treated

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with antibiotics

Supportive care is given (i.e. inotropica, mechanical ventilation,

renal function replacement).

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Anaphylaxis is treated with adrenaline to stimulate cardiac

performance and corticosteroids to reduce the inflammatory

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response.

In neurogenic shock because of vasodilation in the legs, one of

the most suggested treatments is placing the patient in the

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Trendelenburg position, thereby elevating the legs and shunting

blood back from the periphery to the body's core. However,

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since bloodvessels are highly compliant, and expand as result of

the increased volume locally, this technique does not work.

More suitable would be the use of vasopressors.

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178

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TREATMENT

In obstructive shock, the only therapy consists of

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removing the obstruction.

Pneumothorax or haemothorax is treated by inserting

a chest tube.

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Pulmonary embolism requires thrombolysis (to

reduce the size of the clot), or embolectomy (removal

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of the thrombus).

Tamponade is treated by draining fluid from the

pericardial space through pericardiocentesis.

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179

TREATMENT

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In endocrine shock the hormone disturbances are

corrected.

Hypothyroidism requires supplementation by means

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of levothyroxine.

In hyperthyroidism the production of hormone by the

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thyroid is inhibited through thyreostatica, i.e.

methimazole (Tapazole) or PTU (propylthiouracil).

Adrenal insufficiency is treated by supplementing

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corticosteroids

180

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TREATMENT

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181

182

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PROGNOSIS

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The prognosis of shock depends on the underlying

cause and the nature and extent of concurrent

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problems. Hypovolemic, anaphylactic and neurogenic

shock are readily treatable and respond well to

medical therapy. Septic shock however, is a grave

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condition and with a mortality rate between 30% and

50%. The prognosis of cardiogenic shock is even

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worse.

183

Bleeding

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184

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Identification of External Bleeding

Arterial Bleed

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Bright red

What is the

Spurting

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physiology that

Venous Bleed

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explains the

Dark red

differences?

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Steady flow

Capillary Bleed

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Dark red
Oozing

185

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Control of External Bleeding

Direct Pressure

gloved hand

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dressing/bandage

Elevation
Arterial pressure points

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186

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Arterial Pressure Points

Upper extremity: Brachial
Lower extremity: Femoral

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187

Control of External Bleeding

Splinting

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Air splint
Pneumatic antishock garment (MAST)

188

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Control of External Bleeding

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Tourniquets

Final resort when all else fails
Used for amputations - sometimes

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3-4" wide
Write "TK" and time of application on forehead of

patient

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Notify other personnel

189

Control of External Bleeding

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Tourniquets

Do not loosen or remove until definitive care is

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available

Do not cover with sheets, blankets, etc.

190

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Epistaxis

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Nosebleed
Common problem

191

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Epistaxis

Causes

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Fractured skull
Facial injuries
Sinusitis, other URIs
High BP
Clotting disorders

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Digital insertion (nose picking)

192

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Epistaxis

Management

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Sit up, lean forward
Pinch nostrils together
Keep in sitting position
Keep quiet

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Apply ice over nose

193

Internal Bleeding

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Can occur due to:

Trauma
Clotting disorders

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Rupture of blood vessels
Fractures (injury to nearby vessels)

194

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Internal Bleeding

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Can result in rapid progression

to hypovolemic shock and death

195

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Internal Bleeding

Assessment

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Mechanism?
Signs and symptoms of hypovolemia without

obvious external bleeding

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196

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Internal Bleeding

Signs and Symptoms

Pain, tenderness, swelling,

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discoloration at injury site

Bleeding from any body orifice

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197

Internal Bleeding

Signs and Symptoms

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Vomiting bright red blood or coffee ground material
Dark, tarry stools (melena)
Tender, rigid, or distended abdomen

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198


Management

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Secure, maintain airway (ABC's)
High concentration oxygen
Assist ventilations
Control obvious bleeding (consider TraumaDex?)
Stabilize fractures

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Replace Fluids
Prevent loss of body heat
Transport rapidly to appropriate facility

199

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