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)

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
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o
m

s

L

a
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a
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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