Cardiovascular Block

Shock
 Learning outcomes
After reviewing the PowerPoint presentation, lecture notes and associated
material, the student should be able to:
Define shock and state the patho-physiological classification of shock.
Describe cellular effects of adequate tissue perfusion.
Describe changes in blood pressure with hemorrhage.
Discuss the stages of hypovolemic shock.
Explain how stage III hypovolemic shock might result in major organs failure.
State the different compensatory mechanisms during a hypovolemic shock.
Explain the role of the arterial baroreceptor reflex in maintaining flow to the
heart and brain in hemorrhage.
Discuss the endocrine and renal compensatory mechanisms in hypovolemic
shock.
 Definition of shock
Shock may be defined as a pathophysiological state in which there is
widespread, serious reduction of tissue perfusion, which if prolonged,
leads to generalized impairment of cellular function.

Reduction of tissue perfusion  decreased availability of oxygen and

nutrients  cellular hypoxia and energy deficit  generalized
impairment of cellular function  cell death  organ failure  whole
body failure  death.
 Pathways leading to decreased tissue perfusion and shock
Decreased tissue perfusion
can result from
hemorrhage/hypovolemia,
cardiac failure, or
neurologic injury.

Decreased tissue perfusion endogenous cellular products from tissue

and cellular injury can then Endotoxins injury
result in immune and
inflammatory responses.

Alternatively, elaboration Activation of receptors

of microbial products during
infection or release of
endogenous cellular
products from tissue injury
can result in cellular
activation to subsequently
influence tissue perfusion
and the development of
shock.
 What drives the blood along the blood vessels
after it has left the heart?
Systemic arterial
HEART
blood pressure.
 Systemic hypotension
NORMAL BP: 120/80
LOW BP < 90/60 DIASTOLE
Arterial pressure = cardiac output x
systemic vascular resistance

Reduction in either component mmHg 80 mmHg 120

(cardiac output or vascular
resistance) without a compensatory Diastolic BP Systolic BP
elevation of the other will result in
hypotension.

SYSTOLE
Mean systemic arterial BP ~ 93 mmHg
 Causes and classification of shock
CLASSIFICATION CAUSES SYMPTOMS AND SIGNS

hypotension; weak but rapid pulse; cool,

Bleeding (internal/external), dehydration  low blood
Hypovolaemic shock clammy skin; rapid, shallow breathing;
volume  decreased cardiac output  hypotension
anxiety, altered mental state
Heart problems (e.g., myocardial infarction, heart
failure)  decreased contractility  decrease in as for hypovolaemic shock + distended
Cardiogenic shock
stroke volume  decreased cardiac output  jugular veins & may be absent pulse
hypotension
Circulatory obstruction (e.g., constrictive pericarditis,
as for hypovolaemic shock + distended
cardiac tamponade, pulmonary embolism  reduced
Obstructive shock jugular veins & pulsus paradoxus (in cardiac
blood flow to lungs  decreased cardiac output 
tamponade).
hypotension
- Septic shock: infection  release of bacterial toxins
 activation of NOS in macrophages  production of Septic shock: hypotension; fever; warm,
NO  vasodilation  decreased vascular resistance sweaty skin
hypotension

- Anaphylatic shock: allergy (release of histamine 

Anaphylatic shock: skin eruptions;
vasodilation  decreased vascular resistance
Distributive shock breathlessness, coughing; localized edema;
hypotension
weak, rapid pulse

- Neurogenic shock: spinal injury  loss of autonomic

Neurogenic shock: as for hypovolemic except
and motor reflexes  reduction of peripheral
warm, dry skin
vasomotor tone  vasodilation  decrease in
peripheral vascular resistance  hypotension
Stages of shock - General
Stages of hypovolaemic shock
Stages of hypovolaemic shock
STAGE I
COMPENSATORY STAGE
10-15% blood loss

In healthy individuals, acute blood loss of 10 – 15 % of

the normal blood volume (e.g., blood donation) results
in activation of the sympathetic nervous system.

Compensation is achieved acutely by:

Increase in heart rate.
Constriction of the arterioles
Thus, cardiac output is normal or slightly reduced
especially when the patient assumes the erect
position

Symptoms and signs:

Arterial pressure is maintained; pressure decline

when the patient assumes the erect position

Increase in heart rate

Paleness

Anxiety

See opposite figure.

Stages of hypovolaemic shock
STAGE II
PROGRESSIVE STAGE
(maximal mobilization of compensatory mechanisms)

20 – 40% blood loss

When 20-40% of blood volume are lost, cardiac output

cannot be maintained and falls markedly, even in the
recumbent position.

Accordingly, there will be massive activation of the

sympathetic nervous system. This results in:

 intense arteriolar constriction in the vascular beds of

the kidney, gut, and skin  redistribution of blood flow
(i.e., centralization of blood flow) with larger fractions
going to the vital organs (heart and brain) and smaller
fractions going to the kidney, gut, and skin. Despite
intense arteriolar constriction, systolic arterial BP
declines by 10 to 20 mm Hg.

 generalized venoconstriction (increasing blood volume

in the central circulation and tending to sustain venous
return)

Fluid also moves from the interstitial to the intravascular

compartment (i.e., reabsorption of tissue fluids).
Stages of hypovolaemic shock
STAGE II
PROGRESSIVE STAGE, continued

Symptoms, signs, and complications

Systolic arterial blood pressure declines by 10-20 mm Hg

Tachycardia (heart rate increases and pulse is thready

and weak)

Skin is pale and cool (peripheral pallor is common)

Deterioration of the mental state because the brain is

getting less oxygen. Patient looks weak, tired and drowsy.
Patient may show anxiety, aggressiveness, and
restlessness.

Thirst.

Oliguria (urine output is decreased).

Angina may occur in patients who have intrinsic coronary

vascular disease.

pH drops and metabolic acidosis develops due to

increased anaerobic glycolysis.
Stages of hypovolaemic shock STAGE III
REFRACTORY STAGE
Irreversible stage
Decompensated stage

> 40% blood loss

The compensatory mechanisms are maximally mobilized in stage

II. Thus, small additional losses of blood (>40 %) can result in life-
threatening reductions in cardiac output, blood pressure, and
tissue perfusion.

Blood flow to heart, brain and kidney is further reduced 

severe ischemia and irreversible tissue damage  this may result in
impaired organ function and death.

The severe vasoconstriction may itself become a complicating

factor and initiate a vicious cycle.
Impaired coronary perfusion  cardiac ischemia 
depression of cardiac function  further lowering of cardiac
output.
Prolonged renal ischemia  acute tubular necrosis  may
lead to prolonged post-shock renal insufficiency.
Bowel ischemia  breakdown of the mucosal barrier. This
may lead to entry of bacteria and toxins into the circulation.
Reduced blood flow to the vasomoter centers in the
medulla depresses the activity of compensatory reflexes.

Thus, stage III is complicated by major organs failure.

Stages of hypovolaemic shock
STAGE III
REFRACTORY STAGE, continued

> 40% blood loss

The factors that determine the ultimate

outcome include:

Duration of stage III.

Severity of tissue anoxia.
Age and condition of the patient.
 What is Sepsis?

In a NORMAL response to an infection, the inflammatory and

coagulation response is localized to the infection site as the immune
system attacks the pathogen, eliminating it from the body.

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 In Sepsis . . .
The inflammatory and
coagulation response is rapid and
widespread, causing a
dysregulated response
• The body’s reaction to the
pathogen may overwhelm all of
the body’s systems
• Immune systems that are too
strong or too weak are unable to
respond effectively to pathogen
invasion

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 Causes of Sepsis
• Bacterial infections are the most common
• Fungal, parasitic or viral infections can also cause sepsis
• The infection can originate from anywhere in the body and
can cause organ damage to any system of the body
Unknown (1/3 of all sepsis cases) •

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 Most Common Infection Sources

https://www.cdc.gov/vitalsigns/sepsis/index.html

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 Who is at Risk to Develop Sepsis?

Host Factor Age, gender, genetics, comorbidities

Elderly account for 60-85 percent of all cases of severe sepsis o

• Immunosuppression
o Disease related, medications related
• Exposure risk
o Community acquired: pneumonia, urinary, wounds, trauma
o Health care acquired: invasive devices, secondary infections and skin
breakdown
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 Progression of Sepsis
Early identification and treatment
It is crucial to identify septic patients and initiate treatment as early along
the continuum as possible and treat them to avoid developing organ damage
or shock.
:Goal
early identification
here Death can result
MOD
Septic
Severe Sepsis + Refractory (unresponsive) hypotension

Sever S
SIRS + Infection
Shock
Sepsis + End Organ Damage

Seps e
38 C or < 36Sepsi
Temp. >is
SIRS C, HR > 90, RR > 20 or PaCO < 32,
WBCs > 12,000 or < 4,000 or > 10% bands
2

s
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 SIRS
Systemic Inflammatory Response Syndrome

SIRS is a nonspecific inflammatory response to an insult that results

in activation of the immune system. This inflammatory response is
the body’s way of attempting to maintain homeostasis.

SIRS is defined as two or more of the following variables:

• Body temperature < 36oC or > 38oC
• Heart rate > 90 beats per minute
• WBC > 12,000/mm3 or < 4,000/mm3 or > 10% bands
• Respiratory rate > 20 breaths per minute or PaCO2 < 32mmHg

SIRS + infection = sepsis

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 Severe Sepsis
Sepsis + new organ dysfunction = severe sepsis
Organ dysfunction is defined as a condition in which an organ does not
function as expected.

Acute Organ
Dysfunction
Related to
Sepsis

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 Septic Shock
Severe sepsis + refractory hypotension OR
lactate ≥ 4 mmol/L = septic shock
Septic shock is a distributive shock •
Cytokine release leads to a large-scale inflammatory response •
Massive vasodilation o
Increased capillary permeability o
Decreased systemic vascular resistance o
Blood clots form in the microvasculature o
Hypotension reduces tissue perfusion causing tissue o
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hypoxia
 Multiple Organ Dysfunction
Syndrome (MODS)
MODS is altered organ function in an acutely ill patient requiring
medical intervention to achieve homeostasis. Can be the end result of
septic shock.

Sepsis-related organ dysfunction → No organ system is immune

• Respiratory failure
• Liver failure
• Kidney failure
• Heart failure
• Gut permeability
• DIC (disseminated intravascular coagulation)
• Altered mental status
• Brain death
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 Treatment Bundle

Give fluids at
Blood 30 mL/kg if:
initial Reperfusion
cultures x2 Give
Lactate hypotension,
assessment
before antibiotics lactate ≥ 4, or
antibiotics septic shock

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 Blood Cultures
Source control: identify and stop the infection

Why two sets of blood cultures?

Corroboration of matching sets confirms treatment of a true pathogen •
versus a contaminate

The goal is to prevent culture negative severe sepsis (CNSS) and septic
shock
Of 6.8 million severe sepsis admissions, 47 percent were culture •
negative
CNSS was seen as a statistically significant independent predictor of •
death

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 Antibiotics
Antibiotics are the life-saving treatment for an infection

• Every hour antibiotic initiation is delayed increases the risk for

mortality by four to eight percent.
• Antibiotics should be given as soon as possible after blood cultures
are drawn.
Preferably after the second set of cultures; however, if the second set o
is going to be delayed more than 30 minutes, antibiotics should be
.started after the first set
• If more than one antibiotic is ordered, give the broadest-spectrum
antibiotic first. Infuse multiple antibiotics concurrently, if
appropriate.

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 Antibiotics
The MOST important thing you can do
for your septic patient

For every hour delay in

antibiotic administration,
mortality increases 4-8%

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 Lactate

With sepsis, lactate is viewed as a marker of global tissue •

.perfusion
:Lactate has some predictive use •
Sustained > 6 hours, an elevated lactate foreshadows increased o
mortality
Mortality increases as lactate levels increase o
Lactate Level Mortality
0-2.5 mmol/L 4.9 percent mortality
2.5-4.0 mmol/L 9.0 percent mortality
> 4.0 mmol/L 28.4 percent mortality

(Nguyen, et al., 2004; Shapiro, et al., 2005)

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 Severe Sepsis
Sepsis + new organ dysfunction = Severe Sepsis
• To be completed within three hours:
o Draw lactate
o Draw two blood cultures prior to antibiotic administration
o Administer broad-spectrum antibiotic(s)
o Fluid resuscitation of 30mL/kg crystalloid solution (NS or LR)
 SBP <90mmHg or MAP <65 mmHg
 Initial lactate > 4 mmol/L Within timeframe of six hours
before or six hours after time
zero
• If initial lactate > 2 mmol/L, repeat lactate within six hours

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 Septic Shock
Severe sepsis + refractory hypotension OR
lactate ≥ 4 mmol/L = septic shock

• To be completed within three hours:

Same as for severe sepsis o
:To be completed within six hours •
o Repeat lactate if initial lactate was > 2.0
o Start vasopressor if persistent hypotension after fluid bolus
• norepinephrine is preferred
Perfusion assessment •

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 SEP-1 Bundle

Documentation of Tissue Perfusion Reassessment

Provider Provider Provider
documentation of 5 of documentation of one documentation of
8 of the following: of the following: completion of
OR OR perfusion
• Arterial oxygenation • Central venous reassessment:
• Vital signs pressure
• Cardiopulmonary measurement • I have completed a
exam full physical
• Capillary refill exam • Central venous assessment
• Peripheral pulse oxygen • Sepsis reassessment
evaluation measurement completed
• Skin exam • Bedside • Sepsis tissue
• Shock index cardiovascular perfusion
• Urine output ultrasound reassessment
• Result of passive leg completed
raise or fluid
challenge
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 . . . Sepsis is a medical emergency
minutes matter
Remember
Sepsis signs and symptoms
• are highly variable due to an
abnormal, dysregulated
response
• most common response to
infection is fever, although not
everyone has a fever

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