Download MBBS (Bachelor of Medicine, Bachelor of Surgery) 1st Year, 2nd Year, 3rd Year and Final year Surgery 51 Shock And Bleeding PPT-Powerpoint Presentations and lecture notes
Shock and Bleeding
1
A 35-year-old man is admitted with systolic blood pressure (BP)
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?
(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.
(D) They are affected and cause an increased creatinine
clearance.
(E) They are prevented from further damage by a vasopressor.
2
Immediate management of a patient with Multiple
fracture and fluid loss includes the infusion -
Blood
Dextran
Normal saline
Ringer lactate
3
Hypotension
In Adults:
systolic BP 90 mm Hg
mean arterial pressure 60 mm Hg
systolic BP > 40 mm Hg from the patient's
baseline pressure
SHOCK
Inadequate perfusion (blood flow)
leading to inadequate oxygen delivery to
tissues
5
"Hypoperfusion can be
present in the absence of
significant hypotension."
Physiology
Basic unit of life = cell
Cells get energy needed to stay alive by reacting
oxygen with fuel (usually glucose)
No oxygen, no energy
No energy, no life
7
Cardiovascular System
Transports oxygen, fuel to cells
Removes carbon dioxide, waste products for
elimination from body
Cardiovascular system must be able to
maintain sufficient flow through
capillary beds to meet cell's oxygen and
fuel needs
8
Flow = Perfusion
Adequate Flow =
Inadequate Flow =
Adequate Perfusion
Indequate Perfusion
(Hypoperfusion)
Hypoperfusion =
Shock
9
What is needed to maintain perfusion?
Pump
Heart
Pipes
Blood Vessels
Fluid
Blood
10
How can perfusion fail?
Pump Failure
Pipe Failure
Loss of Volume
11
Types of Shock and Their
Causes
12
Cardiogenic Shock
Pump failure
Heart's output depends on
How often it beats (heart rate)
How hard it beats (contractility)
Rate or contractility problems cause pump failure
13
Cardiogenic Shock
Causes
Acute myocardial infarction
Very low heart rates (bradycardias)
Very high heart rates (tachycardias)
Why would a high heart rate caused decreased output?
Hint: Think about when the heart fills.
14
Neurogenic Shock
Loss of peripheral resistance
Spinal cord injured
Vessels below injury dilate
What happens to the pressure in a
closed system if you increase its size?
15
Hypovolemic Shock
Loss of volume
Causes
Blood loss: trauma
Plasma loss: burns
Water loss: Vomiting, diarrhea, sweating, increased
urine, increased respiratory loss
If a system that is supposed to be closed
leaks, what happens to the pressure in it?
16
Psychogenic Shock
Simple fainting (syncope)
Caused by stress, pain, fright
Heart rate slows, vessels dilate
Brain becomes hypoperfused
Loss of consciousness occurs
What two problems combine to produce
hypoperfusion in psychogenic shock?
17
Septic Shock
Results from body's response to bacteria in
bloodstream
Vessels dilate, become "leaky"
What two problems combine to produce
hypoperfusion in septic shock?
18
Anaphylactic Shock
Results from severe allergic reaction
Body responds to allergen by releasing histamine
Histamine causes vessels to dilate and become
"leaky"
What two problems combine to produce
hypoperfusion in anaphylaxis?
19
OBSTRUCTIVE SHOCK
Flow of blood is obstructed.
Cardiac tamponade
Constrictive pericarditis
Tension pneumothorax.
Massive pulmonary embolism
Aortic stenosis.
20
PATHOPHYSIOLOGY OF
SHOCK SYNDROME
Cells switch from aerobic to anaerobic metabolism
lactic acid production
Cell function ceases & swells
membrane becomes more permeable
electrolytes & fluids seep in & out of cell
Na+/K+ pump impaired
mitochondria damage
cell death
COMPENSATORY MECHANISMS: Sympathetic
Nervous System (SNS)-Adrenal Response
Stimulated by baroreceptors
+Increased heart rate
+Increased contractility
+Vasoconstriction (SVR-Afterload)
+Increased Preload
COMPENSATORY MECHANISMS:
Sympathetic Nervous System (SNS)-Adrenal
Response
SNS - Hormonal: Renin-angiotension system
+Decrease renal perfusion
+Releases renin
angiotension I
+angiotension II
potent vasoconstriction &
+releases aldosterone adrenal cortex
+sodium & water retention
COMPENSATORY MECHANISMS:
Sympathetic Nervous System (SNS)-Adrenal
Response
SNS - Hormonal: Antidiuretic Hormone
+Osmoreceptors in hypothalamus stimulated
+ADH released by Posterior pituitary gland
+Vasopressor effect to increase BP
+Acts on renal tubules to retain water
COMPENSATORY MECHANISMS:
Sympathetic Nervous System (SNS)-Adrenal
Response
SNS - Hormonal: Adrenal Cortex
+Anterior pituitary releases adrenocorticotropic
hormone (ACTH)
+Stimulates adrenal Cx to release glucorticoids
+Blood sugar increases to meet increased metabolic
needs
Stages of Shock
?Initial stage - tissues are under perfused, decreased CO,
increased anaerobic metabolism, lactic acid is building
?Compensatory stage - Reversible. SNS activated by low CO,
attempting to compensate for the decrease tissue perfusion.
?Progressive stage - Failing compensatory mechanisms:
profound vasoconstriction from the SNS
ISCHEMIA
Lactic acid production is high
metabolic acidosis
?Irreversible or refractory stage - Cellular necrosis and Multiple
Organ Dysfunction Syndrome may occur
DEATH IS IMMINENT!!!!
Net results of cellular shock:
?systemic lactic acidosis
?decreased myocardial contractility
?decreased vascular tone
?decrease blood pressure, preload, and
cardiac output
Case 1
24 year old male
Previously healthy
Lives in a malaria endemic area (PNG)
Brought in by friends after a fight - he was kicked in
the abdomen
He is agitated, and won't lie flat on the stretcher
HR 92, BP 126/72, SaO2 95%, RR 26
Stages of Shock
Insult
Preshock
(Com
pe
nsa ti
on)
Timeline and progression will
Shockdepend
(Com
pe
nsat i
on -Cause
Ove
rwhel
m e
d) -Patient Characteristics
-Intervention
End organ
Damage
Death
Case 1: Stages of Shock
Stage
Pathophysiology
Clinical Findings
Insult
Splenic Rupture -- Blood Loss Abdominal tenderness and girth
Case 1: Stages of Shock
Stage
Pathophysiology
Clinical Findings
Insult
Splenic Rupture -- Blood Loss Abdominal tenderness and
girth
Preshock Hemostatic compensation
MAP is maintained
MAP =CO(HR xSV) xSVR
HR wil be increased
Decreased CO is compensated by Extremities wil be cool due
increase in HR and SVR
to vasoconstriction
Case 1: Stages of Shock
Stage
Pathophysiology
Clinical Findings
Insult
Splenic Rupture -- Blood
Abdominal tenderness and
Loss
girth
Preshock
Hemostatic compensation MAP is maintained
MAP =CO(HR xSV) x SVR HR wil be increased
Decreased CO is compensated Extremities wil be cool due to
by increase in HR and SVR
vasoconstriction
Shock
Compensatory mechanisms MAP is reduced
fail
Tachycardia, dyspnea,
restlessness
S Ca
tage se
P 1
ath:
o
pS
hyt
sia
ol g
og e
y s of Shoc
Clinical k
Findings
Insult
Splenic Rupture -- Blood Loss Abdominal tenderness and girth
Preshock Hemostatic compensation
MAP is maintained
MAP =CO(HR xSV) x SVR
HR wil be increased
Decreased CO is compensated
Extremities wil be cool due to
by increase in HR and SVR
vasoconstriction
Shock
Compensatory mechanisms
MAP is reduced
fail
Tachycardia, dyspnea,
restlessness
End
Cel death and organ failure
Decreased renal function
organ
Liver failure
dysfuncti
Disseminated Intravascular
on
Coagulopathy
Death
Si
Igns this Shock?
s
a
n
d
s
y
m
p
t
o
m
s
L
a
b
o
r
a
t
o
r
y
f
i
n
d
i
n
g
s
H
e
m
o
d
y
n
a
m
i
c
m
e
a
s
u
r
e
s
Symptoms and Signs of Shock
Level of consciousness
Initially may show few symptoms
Continuum starts with
Anxiety
Agitation
Confusion and Delirium
Obtundation and Coma
In infants
Poor tone
Unfocused gaze
Weak cry
Lethargy/Coma
(Sunken or bulging fontanelle)
Symptoms and Signs of Shock
Pulse
Tachycardia HR > 100 - What are a few exceptions?
Rapid, weak, thready distal pulses
Respirations
Tachypnea
Shallow, irregular, labored
Symptoms and Signs of Shock
Blood Pressure
May be normal!
Definition of hypotension
Systolic < 90 mmHg
MAP < 65 mmHg
40 mmHg drop systolic BP from from baseline
Children
Systolic BP < 1 month = < 60 mmHg
Systolic BP 1 month - 10 years = < 70 mmHg + (2 x age in years)
In children hypotension develops late, late, late
A pre-terminal event
Symptoms and Signs of Shock
Skin
Cold, clammy (Cardiogenic, Obstructive, Hemorrhagic)
Warm (Distributive shock)
Mottled appearance in children
Look for petechia
Dry Mucous membranes
Low urine output <0.5 ml/kg/hr
Empiric Criteria for Shock
4 out of 6 criteria have to be met
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
Lactate > 4
Management of Shock
History
Physical exam
Labs
Other investigations
Treat the Shock - Start treatment as soon as you
suspect Pre-shock or Shock
Monitor
Historical Features
Trauma?
Pregnant?
Acute abdominal pain?
Vomiting or Diarrhea?
Hematochezia or hematemesis?
Fever? Focus of infection?
Chest pain?
Physical Exam
Vitals - HR, BP, Temperature, Respiratory rate,
Oxygen Saturation
Capillary blood sugar
Weight in children
Physical Exam
In a patient with normal level of consciousness -
Physical exam can be directed by the history
Physical Exam
In a patient with abnormal level of consciousness
Primary survey
Cardiovascular (murmers, JVP, muffled heart sounds)
Respiratory exam (crackles, wheezes),
Abdominal exam
Rectal and vaginal exam
Skin and mucous membranes
Neurologic examination
Laboratory Tests
CBC, Electrolytes, Creatinine/BUN, glucose
+/- Lactate
+/- Capillary blood sugar
+/- Cardiac Enzymes
Blood Cultures
Beta HCG
+/- Cross Match
Other investigations
ECG
Urinalysis
CXR
+/- Echo
+/- FAST
Treatment
Start treatment immediately
Stages of Shock
Insult
Preshock
(Com
pe
nsa ti
on)
Early Intervention can arrest or
Shoc k reduce the damage
(Compensation
Overwhelmed)
End organ
Damage
Death
Treatment
ABC's "5 to 15"
Airway
Breathing
Circulation
Put the patient on a monitor if available
Treat underlying cause
Treatment: Airway and
Breathing
Give oxygen
Treatment: Airway and Breathing
Consider Intubation
Is the cause quickly reversible?
Generally no need for intubation
3 reasons to intubate in the setting of shock
Inability to oxygenate
Inability to maintain airway
Work of breathing
Treatment: Circulation
Treat the early signs of shock (Cold, clammy?
Decreased capillary refill? Tachycardic? Agitated?)
DO NOT WAIT for hypotension
Treatment: Circulation
Start IV +/- Central line (or Intraosseous)
Do Blood Work +/- Blood Cultures
Treatment: Circulation
Fluids - 20 ml/kg bolus x 3
Normal saline
Ringer's lactate
Back to Case 1
24 year old male
Previously healthy
Lives in a malaria endemic area (PNG)
Brought in by friends after a fight - he was kicked in
the abdomen
He is agitated, and won't lie flat on the stretcher
HR 92, BP 126/72, SaO2 95%, RR 26
Case 1
On examination
Extremely agitated
Clammy and cold
Heart exam - normal
Chest exam - good air entry
Abdomen - bruised, tender, distended
No other signs of trauma
Case 1: Management
Hemorrhagic (Hypovolemic Shock)
ABC's
Monitors
O2
Intubate?
IV lines x 2, Fluid boluses, Call for Blood - O type
Blood work including cross match
Treat Underlying Cause
Case 1: Management
Hemorrhagic (Hypovolemic Shock)
ABC's
Monitors
O2
Intubate?
IV lines x 2, Fluid boluses, Call for Blood - O type
Blood work including cross match
Treat Underlying Cause
Give Blood
Call the surgeon stat
If the patient does not respond to initial boluses and blood products
- take to the Operating Room
Blood Products
Use blood products if no improvement to fluids
PRBC 5-10 ml/kg
O- in child-bearing years and O+ in everyone else
+/- Platelets
Case 2
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
Case 2
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
Chest - bilateral crackles, accessory muscle use
Abdomen - unremarkable
Rest of exam is normal
Stages of Shock
Insult
Preshock
(Compensation)
What stage is she at?
Shock
(Com pe
nsat i
on
Overwhelmed)
End organ
Damage
Death
Case 2: Management
Cardiogenic Shock
ABC's
Monitors
O2
IV and blood work
ECG - Atrial Fibrillation, rate 130's
Treat Underlying Cause
Case 2: Management
Cardiogenic Shock
ABC's
Monitors
O2
IV and blood work
Intubate?
ECG - Atrial Fibrillation, rate 130's
Treat Underlying Cause
Case 2: Why would you
intubate?
Is the cause quickly reversible?
UNLIKELY
3 reasons to intubate in the setting of shock
Inability to oxygenate
Inability to oxygenate
Inability to maintain airway
(Pulmonary edema,
SaO2 88%)
Work of breathing
Accessory
Muscle Use
Case 2: Why Intubate?
Strenuous use of accessory respiratory muscles (i.e.
work of breathing) can:
Increase O2 consumption by 50-100%
Decrease cerebral blood flow by 50%
Case 2: Management
Cardiogenic Shock
ABC's
Monitors
O2
IV and blood work
Intubate?
ECG - Atrial Fibrillation, rate 130's
Treat Underlying Cause
Case 2: Management
Cardiogenic Shock
Treat Underlying Cause
Lasix
Atrial Fibrillation - Cardioversion? Rate control?
Inotropes - Dobutamine +/- Norepinephrine (Vasopressor)
Look for precipitating causes - infectious?
Vasopressors in Cardiogenic
Shock
Norepinephrine
Dopamine
Epinephrine
Phenylephrine
Case 3
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
Case 3
HR 126, SBP 82, SaO2 70%, RR 36, Temp 35
Obtunded, Accessory muscle use
Trachea is deviated to Left
Heart - distant heart sounds
Chest - decreased air entry on the right, broken ribs,
subcutaneous emphysema
Abdominal exam - normal
Apart from bruises and scrapes no other signs of
trauma
Stages of Shock
Insult
Preshock
(Compensation)
What stage is she at?
Shock
(Com pe
nsat i
on
Overwhelmed)
End organ
Damage
Death
Case 3: Management
Obstructive Shock
ABC's
Monitors
O2
IV
Intubate?
BW
Treat Underlying Cause
Case 3: Management
Obstructive Shock
ABC's
Monitors
O2
IV
Intubate?
BW
Treat Underlying Cause
Needle thoracentesis
Chest tube
CXR
Case 3: Management
Obstructive Shock
ABC's
Monitors
O2
IV
Intubate?
BW
Treat Underlying Cause
Needle thoracentesis
Chest tube
CXR
Case 3: Management
Obstructive Shock
ABC's
Monitors
O2
IV
Intubate?
BW
Treat Underlying Cause
Needle thoracentesis
Chest tube
CXR
Intubate if no response
Case 3
You perform a needle thoracentesis - hear a hissing
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
Case 3
1 hr has gone by
You are having lunch
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
feeling not so good" and leaves.
Case 3
You are back at the bedside
The patient is obtunded again
Pale and Clammy
HR 130, BP 86/52, SaO2 96% on O2
Chest tube seems to be working
Trachea is midline
Heart - Normal
Chest - Good air entry
Abdomen - decreased bowel sounds, distended
Combined Shock
Different types of shock can coexist
Can you think of other examples?
Monitoring
Vitals - BP, HR, SaO2
Mental Status
Urine Output (> 1-2 ml/kg/hr)
When something changes or if you do not observe a
response to your treatment -
re-examine the patient
Can we measure cel hypoxia?
Lactate - we already talked about - a surrogate
Venous Oxygen Saturation - more direct measure
Venous Oxygen Saturation
Hg carries O2
A percentage of O2 is extracted by the tissue for
cellular respiration
Usually the cells extract < 30% of the O2
Venous Oxygen Saturation
Svo2 = Mixed venous oxygen saturation
Measured from pulmonary artery by Swan-Ganz catheter.
v Normal > 65%
Scvo2 = Central venous oxygen saturation
Measured through central venous cannulation of SVC or R Atrium
- i.e. Central Line
v Normal > 70%
PART 2
Case 4
40 year old male
RUQ abdominal pain, fever, fatigued for 5-6 days
No past medical history
Case 4
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
Abdomen - decreased bowel sound, tender RUQ
Stages of Shock
Insult
Preshock
(Compensation)
What stage is he at?
Shock
(Com pe
nsat i
on
Overwhelmed)
End organ
Damage
Death
Stages of Sepsis
SIRS
SEPSIS
SEVERE
SE
PSIS
SEPTIC
SHOCK
MODS/DEATH
Definitions of Sepsis
Systemic Inflammatory Response Syndrome (SIRS) ? 2
or > of:
-Temp > 38 or < 36
-RR > 20
-HR > 90/min
-WBC >12,000 or <6,000 or more than 10%
immature bands
Definitions of Sepsis
Sepsis ? SIRS with proven or suspected
microbial source
Severe Sepsis ? sepsis with one or more signs of
organ dysfunction or hypoperfusion.
Definitions of Sepsis
Septic shock = Sepsis + Refractory
hypotension
-Unresponsive to initial fluids 20-40cc/kg ?
Vasopressor dependant
MODS ? multiple organ dysfunction
syndrome
-2 or more organs
Stages of Sepsis
Mortality
SIRS
7%
SEPSIS
16%
SEVERE
20%
SE
PSIS
SEPTIC
70%
SHOCK
MODS/DEATH
Pathophysiology
Complex pathophysiologic mechanisms
Pathophysiology
Inflammatory Cascade:
Humoral, cellular and Neuroendocrine (TNF, IL etc)
Endothelial reaction
Endothelial permeability = leaking vessels
Coagulation and complement systems
Microvascular flow impairment
Pathophysiology
End result = Global Cellular Hypoxia
Focus of Infection
Any focus of infection can cause sepsis
Gastrointestinal
GU
Oral
Skin
Risk Factors for Sepsis
Infants
Immunocompromised patients
Diabetes
Steroids
HIV
Chemotherapy/malignancy
Malnutrition
Sickle cell disease
Disrupted barriers
Foley, burns, central lines, procedures
Back to Case 4
HR 110, BP 100/72, SaO2 96%, T 39.2, RR 20
Drowsy
Warm skin
Heart - S1, S2, no Murmers
Chest - good A/E x 2
Abdomen - decreased bowel sound, tender RUQ
Case 4: Management
Distributive Shock (SEPSIS)
ABC's
Monitors
O2
IV fluids 20 cc/kg x 3
Intubate?
BW
Treat Underlying Cause
Resuscitation in Sepsis
Early goal directed therapy - Rivers et al NEJM 2001
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.
Emergency patients by emergency doctors
Resuscitation protocol started early - 6 hrs
Resuscitation in Sepsis: EGDT
The theory is to normalize...
Preload - 1st
Afterload - 2nd
Contractility - 3rd
BACK TO OUR EQUATION
MAP = CO x SVR
(HR x Stroke volume)
Preload
Afterload
Contractility
BACK TO OUR EQUATION
MAP = CO x SVR
(HR x Stroke volume)
Preload
Afterload
Contractility
Preload
Dependent on intravascular volume
If depleted intravascular volume (due to increased endothelial
permeability) - PRELOAD DECREASES
Can use the CVP as measurement of preload
Normal = 8-12 mm Hg
Preload
How do you correct decreased preload (or intravascular volume)
Give fluids
Rivers showed an average of 5 L in first 6 hours
What is the end point?
BACK TO OUR EQUATION
MAP = CO x SVR
(HR x Stroke volume)
Preload
Afterload
Contractility
Afterload
Afterload determines tissue perfusion
Using the MAP as a surrogate measure - Keep between 60-90 mm
Hg
In sepsis afterload is decreased d/t loss of vessel tone
Afterload
How do you correct decreased afterload?
Use vasopressor agent
Norepinephrine
Alternative Dopamine or Phenylpehrine
BACK TO OUR EQUATION
MAP = CO x SVR
(HR x Stroke volume)
Preload
Afterload
Contractility
Contractility
Use the central venous oxygen saturation (ScvO2)
as a surrogate measure
Shown to a be a surrogate for cardiac index
Keep > 70%
Contractility
How to improve ScvO2 > 70%?
Optimize arterial O2 with non-rebreather
Ensure a hematocrit > 30 (Transfuse to reach a hematocrit of > 30)
Use Inotrope - Dobutamine 2.5ug/kg per minute and titrated (max 20ug/kg)
Respiratory Support - Intubation (Don't forget to sedate and paralyze)
Suspect infection
EGDT
Document source within 2hrs
The high risk pt: Systolic < 90 after bolus
Or
Lactate > 4mmol/l
Abx within 1 hr
+ source control
<8mm hg
CVP
Crystalloid
Decrease 02
> 8 ?12 mm hg
Consumption
<65 or >90mmhg
MAP
Vasoactive
INTUBATE
agent
> 65 ? 95mm hg
<70%
Scv02
Packed RBC
to Hct >30%
>70%
<70%
>70%
Inotropes
NO
Goals Achieved
Suspect infection
EGDT
Document source within 2hrs
The high risk pt: systolic < 90 after bolus
Or
INTUBATE
Lactate > 4mmol/l
EARLY
IF IMPENDING
Abx within 1 hr
RESPIRATORY
FAILURE
+ source control
<8mm hg
CVP
Crystalloid
Decrease 02
> 8 ?12 mm hg
Consumption
<65 or >90mmhg
MAP
Vasopressor
INTUBATE
> 65 ? 95mm hg
<70%
Scv02
Packed RBC
to Hct >30%
>70%
<70%
>70%
Inotropes
NO
Goals Achieved
Suspect infection
MODIFIED
Document source within 2hrs
The high risk pt: systolic < 90 after bolus
INTUBATE EARLY
IF IMPENDING
RESPIRATORY
Abx within 1 hr
FAILURE
And source control
< 65 mmHg
MAP (Urine
More fluids
Decrease 02
>65 mmHgOutput)
Consumption
<65 mmHg
MAP
Vasopressors
INTUBATE
>65mm hg
< 10 %
Lactate
Packed RBC
Clearance
to Hct >30%
> 10%
< 10%
> 10%
Inotropes
NO
Goals Achieved
Case 4: Management
Distributive Shock (SEPSIS)
ABC's
Monitors
O2
IV fluids 20 cc/kg
Intubate
BW
Treat Underlying Cause
Acetaminophen
Antibiotics - GIVE EARLY
Source control - the 4 D's = Drain, Debride, Device removal,
Definitive Control
Antibiotics
Early Antibiotics
Within 3-6hrs can reduce mortality - 30%
Within 1 hr for those severely sick
Don't wait for the cultures ? treat empirically then
change if need.
Other treatments for severe
sepsis:
Glucocorticoids
Glycemic Control
Activated protein C
Couple of words about Steroids
in sepsis...
New Guidelines for the management of sepsis
and septic shock = Surviving Sepsis Campaign
Grade 2C ? consider steroids for septic shock in patients
with BP that responds poorly to fluid resuscitation and
vasopressors
Critical Care Med 2008 Jan 36:296
Concluding Remarks
Know how to distinguish different types of shock and
treat accordingly
Look for early signs of shock
SHOCK = hypotension
Concluding Remarks
Choose cost effective and high impact interventions
Do not need central lines and ScvO2
measurements to make an impact!!
Concluding Remarks
ABC's "5 to 15"
Can't intubate?
Give oxygen
Develop algorithms for bag valve mask ventilation
Treat fever to decrease respiratory rate
Treat early with fluids - need lots of it!!
Concluding Remarks
Monitor the patient
Do not need central venous pressure and ScvO2
Use the HR, MAP, mental status, urine output
Lactate clearance?
Concluding Remarks
Start antibiotics within an hour!
Do not wait for cultures or blood work
A 22 year old man was driving drunk and without his seatbelt fastened when
he was involved in a
single-vehicle automobile accident. When attended by EMT personnel, no
information was
available about the time of the accident. He was found agitated and
complaining of abdominal
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
and on a back board
and transported to your emergency room. Upon arrival his vital signs are the
same, with a
temperature of 36oC. His abdomen is markedly distended. His hands and feet
are cold, his legs
mottled. A nasogastric tube reveals green liquid. A urinary catheter reveals
dark yellow urine. His
hemoglobin is 7. His abdominal lavage reveals gross blood.
135
Study Questions:
What type of shock does this patient exhibit?
What would be the cardiac output (low, normal,
high)?
What would be the systematic resistance (low,
normal, high)?
What would be the central venous and/or pulmonary
capillary occlusion pressure (low, normal,
high)?
What therapy would reverse the shock?
136
A 65 year old man with known coronary artery disease
(myocardial infarct three years earlier,
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,
temperature 39oC. He is flushed with
warm hands and warm feet, his legs are pink. Physical
examination reveals findings consistent
with peritonitis in the left lower quadrant.
137
Study Questions:
What type of shock does this patient exhibit?
What would be the cardiac output (low, normal,
high)?
What would be the systemic resistance (low, normal,
high)?
What would be the central venous and/or pulmonary
capillary occlusion pressure (low, normal,
high)?
What therapy would reverse the shock?
138
A 35 year old man dove into three feet of water at a
swimming pool, did not emerge and was
rescued by friends who performed CPR. When the EMTs
arrived they found the patient to have a
blood pressure of 80/50, pulse 100, and no spontaneous
respirations, although he was opening his
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
room. Upon arrival he has the same
vital signs with warm hands and feet and pink extremities.
139
STAGES OF SHOCK
140
Types of Shock and Their
Causes
141
Cardiogenic Shock
Pump failure
Heart's output depends on
How often it beats (heart rate)
How hard it beats (contractility)
Rate or contractility problems cause pump failure
142
Cardiogenic Shock
Causes
Acute myocardial infarction
Very low heart rates (bradycardias)
Very high heart rates (tachycardias)
Why would a high heart rate caused decreased output?
Hint: Think about when the heart fills.
143
144
145
Neurogenic Shock
Loss of peripheral resistance
Spinal cord injured
Vessels below injury dilate
What happens to the pressure in a
closed system if you increase its size?
146
Hypovolemic Shock
Loss of volume
Causes
Blood loss: trauma
Plasma loss: burns
Water loss: Vomiting, diarrhea, sweating, increased
urine, increased respiratory loss
If a system that is supposed to be closed
leaks, what happens to the pressure in it?
147
148
Psychogenic Shock
Simple fainting (syncope)
Caused by stress, pain, fright
Heart rate slows, vessels dilate
Brain becomes hypoperfused
Loss of consciousness occurs
What two problems combine to produce
hypoperfusion in psychogenic shock?
149
Septic Shock
Results from body's response to bacteria in
bloodstream
Vessels dilate, become "leaky"
What two problems combine to produce
hypoperfusion in septic shock?
150
Anaphylactic Shock
Results from severe allergic reaction
Body responds to allergen by releasing histamine
Histamine causes vessels to dilate and become
"leaky"
What two problems combine to produce
hypoperfusion in anaphylaxis?
151
OBSTRUCTIVE SHOCK
In this situation the flow of blood is obstructed which
impedes circulation and can result in circulatory arrest.
Several conditions result in this form of shock.
Cardiac tamponade in which fluid in the pericardium prevents
inflow of blood into the heart (venous return). Constrictive
pericarditis, in which the pericardium shrinks and hardens, is
similar in presentation.
Tension pneumothorax. Through increased intrathoracic pressure,
bloodflow to the heart is prevented (venous return).
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.
Aortic stenosis hinders circulation by obstructing the
ventricular outflow tract
152
ENDOCRINE SHOCK
Hypothyroidism, in critically ill patients, reduces cardiac
output and can lead to hypotension and respiratory
insufficiency.
Thyrotoxicosis may induce a reversible cardiomyopathy.
Acute adrenal insufficiency is frequently the result of
discontinuing corticosteroid treatment without tapering the
dosage. However, surgery and intercurrent disease in
patients on corticosteroid therapy without adjusting the
dosage to accommodate for increased requirements may also
result in this condition.
Relative adrenal insufficiency in critically ill patients where
present hormone levels are insufficient to meet the higher
demands .
153
Shock:
Signs and Symptoms
Restlessness, anxiety
Nausea, vomiting
Increased pulse rate
Thirst
Decreasing level of
Diminished urine output
consciousness
Dull eyes
Rapid, shallow respirations
Why are these signs and symptoms present?
Hint: Think hypoperfusion
154
155
156
Shock:
Signs and Symptoms
Hypovolemia will cause
Neurogenic shock will cause:
Weak, rapid pulse
Weak, slow pulse
Pale, cool, clammy skin
Dry, flushed skin
Cardiogenic shock may cause:
Sepsis and anaphylaxis will
Weak, rapid pulse or weak, slow
cause:
pulse
Weak, rapid pulse
Pale, cool, clammy skin
Dry, flushed skin
Can you explain the differences in the
signs and symptoms?
157
Shock: Signs and Symptoms
Patients with anaphylaxis will:
Develop hives (urticaria)
Itch
Develop wheezing and difficulty breathing
(bronchospasm)
What chemical released from the body during an
allergic reaction accounts for these effects?
158
Shock:
Signs and Symptoms
Shock is NOT the same thing
as a low blood pressure!
A falling blood pressure
is a LATE sign of shock!
159
Shock:
Signs and Symptoms
Obscure/Less viewed symptom of shock
Drop in end tidal carbon dioxide (ETCO2) level
Indicative of respiratory failure resulting in poor
oxygenation, therefore, poor perfusion or Shock
160
Severity of shock
Compensated shock
body's cardiovascular and endocrine compensatory
responses reduce flow to non-essential organs to
preserve preload and flow to the lungs and brain.
Apart from a tachycardia and cool peripheries
(vasoconstriction, circulating catecholamines) there
may be no other clinical signs of hypovolaemia.
161
Decompensation
Further loss of circulating volume overloads the
body's compensatory mechanisms and there is
progressive renal, respiratory and cardiovascular
decompensation.
In general, loss of around 15% of the circulating blood
volume is within normal compensatory mechanisms.
Blood pressure is usually well maintained and only
falls after 30?40% of the circulating volume has been
lost.
162
Mild shock
Initially there is tachycardia, tachypnoea and a mild
reduction in urine output and mild anxiety.
Blood pressure is maintained although there is a
decrease in pulse pressure.
The peripheries are cool and sweaty with prolonged
capillary refill times (except in septic distributive
shock).
163
Moderate shock
As shock progresses, renal compensatory mechanisms
fail, renal perfusion falls and urine output dips below
0.5 ml kg?1h?1.
There is further tachycardia and now the blood
pressure starts to fall.
Patients become drowsy and mildly confused.
164
Severe shock
In severe shock there is profound tachycardia and
hypotension.
Urine output falls to zero and patients are
unconscious with laboured respiration
165
Treatment
Secure, maintain airway (ABC's)
High concentration oxygen
Assist ventilations
Control obvious bleeding (consider TraumaDex?)
Stabilize fractures
Replace Fluids
Prevent loss of body heat
Transport rapidly to appropriate facility
166
Treatment
Elevate lower extremities 8 to 12 inches in
hypovolemic shock (Trendelenberg Position)
Do NOT elevate the lower extremities in
cardiogenic shock
Why the difference in
management?
167
Treatment
Administer nothing by mouth, even if the patient
complains of thirst
168
TREATMENT
Immediate intervention, even before a diagnosis is
made.
Re-establishing perfusion to the organs is the primary
goal.
Restoring and maintaining the blood circulating
volume ensuring oxygenation and blood pressure are
adequate, achieving and maintaining effective cardiac
function, and preventing complications. )
Intubation and mechanical ventilation may be
necessary.
169
In hypovolemic shock, caused by bleeding, it is necessary to
immediately control the bleeding and restore the casualty's blood
volume by giving infusions of isotonic crystalloid solutions. Blood
transfusions, packed red blood cells (RBCs), Albumin (or other colloid
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,
diarrhea, vomiting, etc. is treated with infusions of electrolyte
solutions that balance the nature of the fluid lost. Sodium is essential
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
delivery of oxygen to the tissues, and mirrors the severity of the shock.
It is best treated by rapidly restoring intravascular volume and
perfusion as above. Inotropic and vasoconstrictive drugs should be
avoided, as they may interfere in knowing blood volume has returned
to normal
170
TREATMENT
In hypovolemic shock, caused by bleeding, it is
necessary to immediately control the bleeding and
restore the casualty's blood volume by giving
infusions of isotonic crystalloid solutions.
Blood transfusions, packed red blood cells (RBCs),
Albumin (or other colloid solutions), or fresh-frozen
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
treated with infusions of electrolyte solutions that
balance the nature of the fluid lost.
171
TREATMENT
Opinion varies on the type of fluid used in shock. The most common
are:
Crystalloids - Such as sodium chloride (0.9%), or Lactated Ringer's.
Dextrose solutions which contain free water are less effective at re-
establishing circulating volume, and promote hyperglycaemia.
Colloids - For example, polysaccharide (Dextran), polygeline
(Haemaccel), succunylated gelatin (Gelofusine) and hetastarch
(Hepsan). Colloids are, in general, much more expensive than
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
crystalloids can further exacerbate the problem and suggest the
combination of crystalloid and colloid solutions.
Blood - Essential in severe hemorrhagic shock, often pre-warmed and
rapidly infused.
172
TREATMENT-HAEMORRHAGIC
SHOCK
It is to be noted that NO plain water should be given
to the patient at any point, as the patient's low
electrolyte levels would easily cause water
intoxication, leading to premature death.
An isotonic or solution high in electrolytes should be
administered if intravenous delivery of recommended
fluids is unavailable.
173
TREATMENT-HAEMORRHAGIC
SHOCK
Vasoconstrictor agents have no role in the initial
treatment of hemorrhagic shock, due to their relative
inefficacy in the setting of acidosis.
Definitive care and control of the hemorrhage is
absolutely necessary, and should not be delayed.
174
TREATMENT-CARDIOGENIC
SHOCK
In cardiogenic shock, depending on the type of
myocardal infarction, one can infuse fluids or in shock
refractory to infusing fluids, inotropic agents.
Inotropic agents, which enhance the heart's pumping
capabilities, are used to improve the contractility and
correct the hypotension.
Should that not suffice, an intra-aortic balloon pump
can be considered (which reduces the workload for
the heart and improves perfusion of the coronary
arteries) or a left ventricular assist device (which
augments the pump-function of the heart.)
175
TREATMENT CARDIOGENIC
SHOCK
The main goals of the treatment of cardiogenic shock
are the re-establishment of circulation to the
myocardium, minimising heart muscle damage and
improving the heart's effectiveness as a pump.
This is most often performed by percutaneous
coronary intervention and insertion of a stent in the
culprit coronary lesion or sometimes by cardiac
bypass.
176
TREATMENT
The main way to avoid the deadly consequence of
death is to make the blood pressure rise again with:
fluid replacement with intravenous infusions
use of vasopressing drugs (e.g. to induce
vasoconstriction);
use of anti-shock trousers that compress the legs and
concentrate the blood in the vital organs (lungs, heart,
brain).
use of blankets to keep the patient warm - metallic
PET film emergency blankets are used to reflect the
patient's body heat back to the patient
177
TREATMENT
In distributive shock caused by sepsis the infection is treated
with antibiotics
Supportive care is given (i.e. inotropica, mechanical ventilation,
renal function replacement).
Anaphylaxis is treated with adrenaline to stimulate cardiac
performance and corticosteroids to reduce the inflammatory
response.
In neurogenic shock because of vasodilation in the legs, one of
the most suggested treatments is placing the patient in the
Trendelenburg position, thereby elevating the legs and shunting
blood back from the periphery to the body's core. However,
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.
178
TREATMENT
In obstructive shock, the only therapy consists of
removing the obstruction.
Pneumothorax or haemothorax is treated by inserting
a chest tube.
Pulmonary embolism requires thrombolysis (to
reduce the size of the clot), or embolectomy (removal
of the thrombus).
Tamponade is treated by draining fluid from the
pericardial space through pericardiocentesis.
179
TREATMENT
In endocrine shock the hormone disturbances are
corrected.
Hypothyroidism requires supplementation by means
of levothyroxine.
In hyperthyroidism the production of hormone by the
thyroid is inhibited through thyreostatica, i.e.
methimazole (Tapazole) or PTU (propylthiouracil).
Adrenal insufficiency is treated by supplementing
corticosteroids
180
TREATMENT
181
182
PROGNOSIS
The prognosis of shock depends on the underlying
cause and the nature and extent of concurrent
problems. Hypovolemic, anaphylactic and neurogenic
shock are readily treatable and respond well to
medical therapy. Septic shock however, is a grave
condition and with a mortality rate between 30% and
50%. The prognosis of cardiogenic shock is even
worse.
183
Bleeding
184
Identification of External Bleeding
Arterial Bleed
Bright red
What is the
Spurting
physiology that
Venous Bleed
explains the
Dark red
differences?
Steady flow
Capillary Bleed
Dark red
Oozing
185
Control of External Bleeding
Direct Pressure
gloved hand
dressing/bandage
Elevation
Arterial pressure points
186
Arterial Pressure Points
Upper extremity: Brachial
Lower extremity: Femoral
187
Control of External Bleeding
Splinting
Air splint
Pneumatic antishock garment (MAST)
188
Control of External Bleeding
Tourniquets
Final resort when all else fails
Used for amputations - sometimes
3-4" wide
Write "TK" and time of application on forehead of
patient
Notify other personnel
189
Control of External Bleeding
Tourniquets
Do not loosen or remove until definitive care is
available
Do not cover with sheets, blankets, etc.
190
Epistaxis
Nosebleed
Common problem
191
Epistaxis
Causes
Fractured skull
Facial injuries
Sinusitis, other URIs
High BP
Clotting disorders
Digital insertion (nose picking)
192
Epistaxis
Management
Sit up, lean forward
Pinch nostrils together
Keep in sitting position
Keep quiet
Apply ice over nose
193
Internal Bleeding
Can occur due to:
Trauma
Clotting disorders
Rupture of blood vessels
Fractures (injury to nearby vessels)
194
Internal Bleeding
Can result in rapid progression
to hypovolemic shock and death
195
Internal Bleeding
Assessment
Mechanism?
Signs and symptoms of hypovolemia without
obvious external bleeding
196
Internal Bleeding
Signs and Symptoms
Pain, tenderness, swelling,
discoloration at injury site
Bleeding from any body orifice
197
Internal Bleeding
Signs and Symptoms
Vomiting bright red blood or coffee ground material
Dark, tarry stools (melena)
Tender, rigid, or distended abdomen
198
Management
Secure, maintain airway (ABC's)
High concentration oxygen
Assist ventilations
Control obvious bleeding (consider TraumaDex?)
Stabilize fractures
Replace Fluids
Prevent loss of body heat
Transport rapidly to appropriate facility
199
This post was last modified on 08 April 2022