PST2235 Module 4 Shock and Haemodynamic Stability

Edith Cowan University
School of Medical Sciences
PST2235: Medical Studies for Paramedics 1
Module 4
Shock and Haemodynamic Stability
Module Objectives
• By the end of this module students should be able to:
• Define shock.
• Outline the factors necessary to achieve adequate tissue
oxygenation.
• Describe how the diameter of resistance vessels influences
preload.
• Calculate mean arterial pressure when given a blood pressure.
• Outline changes in the microcirculation during the progression of
shock.
• List the causes of hypovolaemic, cardiogenic, neurogenic,
anaphylactic, and septic shock.
Module Objectives
• By the end of this module students should be able
to:
• Describe and explain pathophysiology as a basis for signs
and symptoms associated with the progression through the
stages of shock.
• Describe key assessment findings that distinguish the
aetiology of the shock state.
• Outline pre-hospital management of the shock patient.
• Describe the principles of fluid administration in shock.
• Define and discuss pharmacological measures that can be
used to manage haemodynamics.
KEY TERMS
• Shock • Haemodilution
• Perfusion • Haemostasis
• Hypoperfusion • Peripheral Vasculature
• Cardiac Output Resistance
• Colloid Solution • Pulse Pressure
• Compensated Shock • Viscosity
• Uncompensated Shock
• Cardiac Cycle
• Irreversible Shock
• Transcapillary Refill
• Crystalloid Solution
• Leaky Capillary Syndrome
• Disseminated Intravascular
Coagulation • Rouleaux Formations
SHOCK - DEFINITION
• Shock was first defined in the 1850’s a:
• “a rude unhinging of the machinery of life”
• We now have a more scientific and specific definition:
• SHOCK: the inability of the circulation to

adequately perfuse the tissues of the body
• A generalised state of hypoperfusion
SHOCK - DEFINITION
• It is important to remember that shock is not a single event.
• Whilst there may be one specific cause, the overall

condition involves a complex group of physiological
abnormalities.
• Therefore: shock can not be adequately defined by pulse

rate, blood pressure, blood loss or cardiac function alone!
• A good Paramedic must take a ‘global’ approach and have

a solid understanding of both cellular and systemic
physiology.
PERFUSION
• PERFUSION: the ability of the body to adequately
circulate blood and provide oxygen to cells.
• HYPOPERFUSION: any malfunction that causes a

decrease in cellular oxygenation.
• When discussing shock, we are really discussing the

perfusion status of the body.
• Simply: Perfusion is everything!!

PERFUSION
• Think: What does a well-perfused patient look like?

What about a poorly-perfused patient?
TISSUE OXYGENATION
• To achieve adequate perfusion, three components of
cardiovascular system must work properly:
• Heart: must sufficiently pump fluid
• Vasculature: must maintain integrity and enable

blood flow
• Lungs: must adequately on/off-load oxygen

TISSUE OXYGENATION - HEART

• Cardiac output: is the amount of blood pumped by the ventricles
in one minute. It is a crucial determinant of organ perfusion.
• It depends on the following:

• Strength of contraction
• Rate of contraction
• Volume of venous return to the ventricles (preload)
• The formula used to determine cardiac output is:
Cardiac output (CO) = Heart rate (HR) × Stroke volume (SV)
• eg: CO = 80 (bpm) × 70 (ml) = 5600 ml/min


• When discussing circulatory involvement in shock,
three key terms are most important:
• PRELOAD
• AFTERLOAD
• MEAN ARTERIAL PRESSURE


• Preload: the amount of blood returning to the
ventricles; it is the end-diastolic volume (EDV).
• It is the ‘load’ that is given to the left ventricle before

contraction.
• EDV has a direct effect on the stretch of the

myocardial sarcomeres- hence the contractility of the
heart via “Starling’s Law”.

• Afterload: the total
resistance against which
blood must be pumped.
• It is the ‘load’ that the heart

must overcome to push
blood out to the body.
• It is directly affected by total

peripheral vascular
resistance.

• Mean Arterial Pressure (MAP): is the mean value of the
blood pressure in the arterial portion of the circulation.
• It represents the average pressure of the vasculature system

that perfuses the cells of the body.
• The formula used to determine MAP is:
MAP = diastolic pressure + 1/3 pulse pressure

• eg: In a patient with BP 120/80
• MAP = 80 + ([120 - 80] / 3) = 80 + (40 / 3) = 80 + 13.3 = 93.3
• Note: Pulse Pressure= systolic minus diastolic.

QUESTION TIME….?
• Why is MAP an important consideration for
Paramedics?
• What is the formula for calculating cardiac output?
• What three factors determine cardiac output?
• Define perfusion.
• Define shock.
CAPILLARY - CELLULAR RELATIONSHIP IN SHOCK
• The progression of shock in microcirculation follows a

sequence of stages related to:
• Changes in capillary perfusion
• Cellular necrosis
• There are four stages:

• Vasoconstriction
• Capillary and venule opening
• Disseminated intravascular coagulation (DIC)
• Multiple organ failure
VASOCONSTRICTION
• In response to hypovolaemia, pre-capillary arterioles and post-
capillary venules constrict
• This constriction helps to maintain systemic BP
• Due to the narrowing of the entrance to the microcirculation, the

velocity of blood passing through it increases (imagine a hose that is
‘pinched’ at the opening, ‘spraying’ into the microcirculation)
• This leads to an increase in hydrostatic pressure in capillaries and

allows fluid to be reabsorbed back into circulation
• Fluid is reabsorbed as it shifts from extravascular space: this is called

transcapillary refill.
VASOCONSTRICTION
As shock progresses:
1. O2 and nutrient delivery to cells by capillaries

decreases
2. Anaerobic metabolism replaces aerobic metabolism
3. Increases the production of H+ and lactate
4. Capillary lining begins to lose it’s ability to contain large
molecules
5. Allows protein-containing fluid to leak into interstitial
spaces
6. This is referred to as leaky capillary syndrome
VASOCONSTRICTION
• Arteriovenous shunts
(anastomosis) will then open-
particularly in the skin, kidneys
and GI tract
• This reduces the pressure on

capillaries
• Sympathetic stimulation
produces:
• Pale, sweaty skin
• Rapid, thready pulse
• Elevation in blood glucose
VASOCONSTRICTION
• Finally, the release of adrenaline dilates coronary,
cerebral, and skeletal muscle arterioles and constricts
other arterioles
• As a result:
• blood is shunted to heart, brain, skeletal muscle
• Capillary flow to kidneys and abdominal organs
decreases
• The vasoconstriction stage of shock must be treated by

prompt restoration of circulatory fluid volume.
CAPILLARY AND VENULE OPENING

• Failure to properly treat shock during vasoconstriction
will cause pre-capillary sphincters to relax.
• This results in some expansion of vascular space
• However, post-capillary sphincters will resist these

relaxation effects, remaining closed.
• This causes:
• blood to pool or stagnate in the capillary system
• capillaries to become engorged with fluid

• This pooling, coupled with arterial hypotension, secondary arteriolar
vasoconstriction and the opening of arteriovenous shunts
contributes to the stagnation of blood flow in capillaries.
• Vascular space continues to expand as increasing hypoxaemia and

acidosis lead to opening of more venules and capillaries.
• Normal blood volume inadequate to fill the “container”
• The capillary and venule capacity can increase so much that the
volume of blood returning to the great veins and venae cava is
significantly reduced, causing a fall in cardiac output.

• Sluggish blood flow and a decrease in the amount of
nutrients to cells causes anaerobic metabolism, which
results in metabolic acidosis.
• As acidosis increases (pH falls), red blood cells begin to

cluster in Rouleaux formations, causing further
decreased perfusion and hyper-coagulation.
• This stage of shock can easily progress further if fluid

resuscitation is inadequate or delayed.
Rouleaux Formations
DISSEMINATED INTRAVASCULAR COAGULATION
• Due to decreases in flow, blood begins to

coagulate in the microcirculation. This is referred
to as:
Disseminated Intravascular Coagulation (DIC)
DISSEMINATED INTRAVASCULAR COAGULATION
• As shock continues, lactic acid accumulates around cells

• Cells no longer have the energy needed to maintain
homeostasis, causing :
• Water and sodium to leak into the cell
• Potassium to leak out
• Cells swell and die (known as the “washout phase”)
• Small areas of dead cells (micro-infarcts) develop in organs

• Pulmonary capillaries become permeable to fluid, leading to
• pulmonary oedema
• decreased absorption of O2
• respiratory failure
MULTIPLE ORGAN FAILURE

• If shock and DIC continue untreated, multiple organ failure will result;
• If an area of capillary occlusion persists for more than 1-2 hours, cells
nourished by that capillary undergo changes that rapidly become
irreversible.
• This cellular necrosis causes the ‘death’ of each organ, however the
amount of necrosis required to produce organ failure varies.
• This depends on the underlying condition of the organ, however:

• hepatic failure usually occurs first
• followed by renal failure and heart failure
MULTIPLE ORGAN FAILURE

Once major organs begin to fail, large systemic changes become
noticeable:
• BP falls dramatically (to levels of 60 mm Hg or less)

• liver and kidney failure is common and often presents early
• capillary blockage causes heart failure
• GI bleeding and sepsis can result from GI mucosal necrosis
• pancreatic necrosis can lead to further clotting disorders and
severe pancreatitis
• Pulmonary thrombosis can produce haemorrhage and fluid loss
into alveoli, which can lead to death from respiratory failure
QUESTION TIME…
• Why do patients in the early stages of shock have

pale, sweaty skin and a rapid, thready pulse?
• Define DIC. What causes this condition?
• What are Rouleaux formations?
• What causes organ failure in Shock?

STAGES OF SHOCK
An understanding of the capillary-cellular relationship in
shock allows for these broad categorisations:
• Compensated shock: there is some decreased

blood flow and perfusion to tissues
• Decompensated shock: compensatory mechanisms

fail and SBP can no longer be maintained.
• Irreversible shock: there is cellular ischaemia and

necrosis and subsequent organ failure.
COMPENSATED SHOCK
• Compensatory mechanisms are sufficient to maintain blood
pressure and therefore perfusion
• Respiratory rate often increases in response to increases in acid

loading
• Signs and symptoms of the COMPENSATED SHOCK patient:

• CNS: mild alteration in conscious state, lethargy, confusion,
combativeness
• Skin: pale, and cool
• Cardio: elevation of heart rate and increase in systolic pressure
COMPENSATED SHOCK
DECOMPENSATED SHOCK
Compensatory mechanisms fail, pre-capillary sphincters open and post-
capillary sphincters remain closed, causing:
• peripheral pooling of blood,
• capillary engorgement & plasma leakage
• decreases in systolic BP
• decreased myocardial contractility due to ischaemic injury
• dysrhythmias
• acidosis
• Rouleaux formations, capillary obstruction & hypercoagulability
• electrolyte imbalances such hyperkalaemia
• heart rate increases
DECOMPENSATED SHOCK
IRREVERSIBLE SHOCK
• Shock progresses and becomes resistant to treatment
• Post-capillary sphincters open allowing toxic by-products to
enter the systemic circulation
• There is profound acidosis organ failure
• Widespread vasodilation= massive decreases in systolic
diastolic BP
Tissue necrosis causes:
• inflammatory changes
• disseminated intravascular coagulation
• multiple organ death
IRREVERSIBLE SHOCK
Clinical signs of irreversible
shock
• Bradycardia
• Serious dysrhythmias
• Frank hypotension
• Evidence of multiple organ
failure
• Pale, cold, clammy skin
Cardiopulmonary collapse is
imminent
IRREVERSIBLE SHOCK
QUESTION TIME…
• Give three signs or symptoms of irreversible shock.
• Rouleaux formations and capillary obstruction occur in

which stage of shock?
• Give signs and symptoms for the following systems in

relation to compensated shock:
• CNS:
• Skin:
• Cardio:
CLASSIFICATIONS OF SHOCK
• The classification of shock is based on the initiating

cause.
• Keep in mind that two or more classifications can often

be combined
• However, remember that the underlying defect is

always inadequate tissue perfusion!
CLASSIFICATIONS OF SHOCK
There are five general classifications of shock:
• Hypovolaemic
• Cardiogenic
• Neurogenic
• Anaphylactic
• Septic
HYPOVOLAEMIC SHOCK
HYPOVOLAEMIC SHOCK: is shock that occurs as

the result of fluid loss.
• Most often it is caused by haemorrhage, however

it can also result from dehydration.
• Shock is always assumed to be hypovolaemic in

nature until proven otherwise!
HYPOVOLAEMIC SHOCK
Causes of hypovolaemic shock
include:
• Haemorrhage
• Burns
• Severe or prolonged diarrhoea
• Vomiting
• Endocrine disorders
• Internal third space losses-
such as in peritonitis
HYPOVOLAEMIC SHOCK
CARDIOGENIC SHOCK
• CARDIOGENIC SHOCK: is shock that occurs due to the

inability of the heart (cardiac pump) to deliver adequate
circulating blood volume for tissue perfusion
• Causes of cardiogenic shock include:

• Inadequate filling of the heart
• Poor contractility of the heart
• Obstruction of blood flow from heart to the central
circulation
CARDIOGENIC SHOCK
Patients in cardiogenic shock may have:
• Acute MI
• Serious cardiac rhythm disturbance
• Cardiac tamponade
• Tension pneumothorax
• Cardiac contusion
• Severe valvular heart disease
• Cardiomyopathy
• Pulmonary embolism
• Dissecting aortic aneurysm
CARDIOGENIC SHOCK
NEUROGENIC SHOCK
NEUROGENIC SHOCK: is shock that occurs due to vasomotor paralysis
below the level of spinal injury.
• Also known as spinal cord, distributive, or vasogenic shock.
• It is caused by the loss of normal vasomotor tone throughout the

sympathetic nervous system
• Loss of sympathetic impulses cause widespread vasodilation,

therefore increasing the size of the “container”
• Even normal intravascular volume is inadequate to fill enlarged

vascular compartment and perfuse tissues= relative hypotension.
NEUROGENIC SHOCK
ANAPHYLACTIC SHOCK
ANAPHYLACTIC SHOCK: is shock that occurs due to the body
being exposed to an antigen that produces a severe allergic reaction
• The body responds to the release of histamines and other mediators

which act on systemic and pulmonary receptors.
• Histamines cause:
• arterioles and capillaries to dilate
• increases in capillary membrane permeability
• intravascular fluid leaks into interstitial space = decrease in
intravascular volume
• constriction of upper and lower airways
• secondary potential for complete airway obstruction
ANAPHYLACTIC SHOCK
Common causes of anaphylactic shock include:
• Medications- especially antibiotic agents such as

penicillin
• Venoms- snakes, spiders, etc.
• Insect stings- bees, wasps
• Food allergies- peanuts, shellfish
• X-ray contrasts
ANAPHYLACTIC SHOCK
SEPTIC SHOCK
• SEPTIC SHOCK: is shock that occurs due to serious systemic
bacterial infections which compromise the integrity of the
circulatory system.
• Septic shock is thought to be caused by:

• toxins that are part of microorganism (endotoxin–gram-
negative sepsis) or
• toxins released by the organism (exotoxin–gram-positive
shock)
• These toxins stimulate the release of complex vasoactive agents

which affect arterioles, capillaries and venules causing
widespread vasodilation and permeability.
SEPTIC SHOCK
• Septic shock is often associated with the following:
• Staphylococcal and streptococcal infections

• Pneumonia
• Postoperative infections
• Infections from indwelling urinary catheters
• Elderly patients
• Immuno-compromised patients
SEPTIC SHOCK
QUESTION TIME…?
• Why does cardiogenic shock develop in a patient who
has had a severe myocardial infarction?
• What secondary problems can arise from anaphylactic

shock?
• Explain the causes of neurogenic shock.
• Give 5 possible causes of hypovolaemic shock.
• Name 3 types of patient who may be susceptible to

septic shock.
SHOCK ASSESSMENT
• Having a thorough, systematic approach to evaluating and

managing shock is essential.
• ALWAYS follow the A-E mnemonic, correcting any life-

threatening irregularities.
• ALWAYS maintain a high index of suspicion in patients

showing any s/s of shock: it is much better to be over-
cautious and safe than sorry!
SHOCK ASSESSMENT: A-E

• A: AIRWAY: must be open, patent and protected
• B: BREATHING: respiratory patterns often reflect the adequacy of

ventilation and can offer clues to the presence of shock. Closely monitor
pulse oximetry.
• C: CIRCULATION: assess circulatory status thoroughly and prioritise

uncontrolled bleeding. Internal bleeding should be suspected in any patient
with signs of shock.
• D: DISABILITY: a rapid assessment of GCS is essential to assess cerebral

perfusion.
• E: EXPOSURE: close visual inspection can reveal conditions that may be life
threatening: get down to the skin!
SHOCK ASSESSMENT: SPECIFIC CONSIDERATIONS
• CIRCULATION: BLEEDING
• In cases of external haemorrhage, apply direct pressure
• Internal bleeding should be suspected in any trauma
patient with signs of shock- especially trauma patients
without evidence of external blood loss
• Treatment must be directed at definitive care to stop
bleeding:
• Rapid transport to definitive care is critical
• IV fluid therapy should be performed en-route to
avoid delay of definitive care
• CIRCULATION: PERFUSION STATUS

• Evaluate rate, character and location of pulses as part
of circulatory assessment
• Remember that pulse rates typically increase
(compensation) early in shock. Strength of cardiac
contraction may also increase (indicated by strength of
pulse)
• Rapid tachycardia may not occur until patient has
suffered 10 to 15 % volume depletion (relative to
container size)
• CIRCULATION: PERFUSION STATUS

• Remember that skin quality and Capillary Refill Test (CRT)
also indicate perfusion status.
• Tissue perfusion can be estimated by evaluating colour,
moisture and temperature of skin
• BUT: be aware that it can be unreliable in:
• Older patients
• Those who have been exposed to extremes of
temperature
• Those suffering from septicaemia and shock caused by
neurological injury
• DISABILITY: NEUROLOGICAL STATUS

• Evaluation of GCS is crucial in assessing cerebral perfusion
• S/s of poor cerebral perfusion include:
• restlessness
• agitation
• confusion
• aggression
• Any significant change in a patient’s GCS or senses should be

considered an indicator of critical perfusion deficit
SHOCK ASSESSMENT: DIFFERENTIAL Dx
• RULE #1: Shock should be assumed to be hypovolaemic

until proven otherwise!
• Diff Dx: Cardiogenic shock
• Chief complaint: chest pain, dyspnoea, tachycardia,

bradycardia or other dysrhythmias
• Signs of congestive heart failure such as jugular vein
distention

• Diff Dx: Neurogenic, Anaphylactic, Septic shock:
• History or scene assessment may reveal mechanism that

suggests vasodilation as cause of shock state
• Signs and symptoms that are unusual in presence of

hypovolaemic shock include warm flushed skin (especially
in dependent areas)
• Those of neurogenic shock include normal pulse rate

(relative bradycardia)

RESUSCITATION
• The underlying treatment philosophy for shock patients is aimed
at quickly ‘resuscitating’ adequate systemic perfusion.
• Every shock patient (apart from cardiogenic shock) requires a

volume expander as part of this process to ensure the ‘container’
is full.
• The type of fluid needed depends on the nature and extent of

volume loss, there are two main categories:
• Crystalloid Solutions
• Colloid Solutions
CRYSTALLOIDS
• CRYSTALLOID SOLUTIONS: are created by dissolving crystals such as salts and sugars
in water
• They do not have as much osmotic pressure as colloid solutions and can be expected
to equilibrate more quickly between vascular and extravascular spaces
• Crystalloids cannot restore the oxygen-carrying capacity of blood!
• 2/3 of infused crystalloid leaves the vascular space within 1 hour

• Therefore: 3 mL is needed to replace 1 mL of blood
• Examples of crystalloids include:
• Hartman’s solution
• Normal saline
• Glucose solutions in water (eg: Dextrose)
CRYSTALLOIDS
• Normal Saline: an isotonic solution that contains sodium and chloride and
replaces volume.
• DOSE: A: 20ml/kg IV/IO to maintain cerebral perfusion
• DOSE: P: 20ml/kg IV/IO to maintain SBP on age range
• Hartman’s Solution: a balanced isotonic solution containing chemicals

found in plasma including potassium, calcium, sodium, chloride and
lactate.
• Electrolyte composition resembles normal plasma, therefore limiting
ion and water movement.
• Preferred in hypovolaemic patients.
• DOSE: A: 20ml/kg IV/IO to maintain cerebral perfusion
• DOSE: P: 20ml/kg IV/IO to maintain SBP on age range
CRYSTALLOIDS
• Glucose Solutions: “Dextrose”: a solution of glucose (sugar)

and water presented in various strength ratios
• Commonly used for hypoglycaemia, however does have
short-acting volume expansion effects (not indicated).
• Dextrose 10%:
• DOSE: A: 10-15 gm IV/IO followed by NaCl flush.
• DOSE: P: 5-10 gm IV/IO followed by NaCl flush.
COLLOIDS
• COLLOID SOLUTIONS: contain molecules (eg: proteins) that are too
large to pass through the capillary membrane.
• They exhibit osmotic pressure and remain within the vascular

compartment for a considerable time.
• Colloids are generally reserved for in-hospital use only.
• Examples of colloid solutions:

• whole blood
• packed red blood cells
• blood plasma
QUESTION TIME…?
• What is the difference between Normal Saline and Hartman’s
Solution?
• What is the #1 Rule of shock?
• What chief complaints may a patient in cardiogenic shock

have?
• Why is skin perfusion an unreliable indicator in elderly

patients?
• List four s/s that might indicate poor cerebral perfusion.

SHOCK MANAGEMENT
• KEY PRINCIPLES OF SHOCK MANAGEMENT
• Establish and maintain open airway: administer high-concentration

O2,assist ventilations
• Control external bleeding
• Initiate IV fluid: two large-bore IV lines of volume-expanding fluid
• Maintain normal body temperature: patients in shock often are unable
to conserve body heat and can become hypothermic easily
• Position: In absence of spine or head injury and if hypovolaemia is
suspected, consider positioning patient in with legs raised
• Monitor: cardiac rhythm and O2 saturation
• Reassess: frequently reassess vital signs en-route
SHOCK MANAGEMENT
VASOACTIVE DRUGS
• In conjunction with fluid resuscitation, there are also
pharmacological means for maintaining perfusion and managing
shock.
• This is done by using vasoactive drugs to increase peripheral

vascular resistance or rate and quality of cardiac contraction.
• These drugs include:

• Adrenaline
• Vasopressin
• Noradrenaline
• Dobutamine
• Atropine
ADRENALINE
• ADRENALINE: a naturally-occurring catecholamine that acts
on the autonomic (sympathetic) nervous system.
• Stimulates alpha and beta adrenergic receptors:

• Alpha: increases vascular tone= raises BP
• Beta: increases heart activity, causes bronchial dilation
• Commonly used in cardiac arrest and post-resuscitation care

mostly for it’s alpha effects.
• Adrenaline degrades continually in the body, therefore

continuous small dose administration is necessary.
ADRENALINE
Cardiac effects of Adrenaline include:
• Increased
• heart rate (chronotropic beta 1 effect)
• contraction strength (inotropic beta 1 effect)
• conduction velocity (dromotropic beta 1 effect)
• vascular resistance from alpha stimulation
• blood pressure due to increased systemic vascular resistance and
cardiac output (mixed beta and alpha effects)
• coronary and cerebral perfusion during CPR (alpha)
• electrical activity in the heart (beta 1 effect)
• myocardial oxygen demand (due to myocardium working harder)
VASOPRESSIN
• VASOPRESSIN: a naturally-occurring antidiuretic hormone that also
causes vascular smooth-muscle contraction
• Activates vasopressin receptors to:

• Vasopressin-1: increase smooth muscle tone to elevate systemic
vascular resistance
• Vasopressin-2: increase water reabsorption in the kidneys
• Used as an alternative to adrenaline during initial management of VF in

the cardiac arrest patient.
• Also utilised as a vasoconstrictive agent in haemodynamically unstable

shock (eg: septic), refractory to more traditional treatments.
NORADRENALINE
• NORADRENALINE: a naturally-occurring catecholamine that is similar
to adrenaline and has potent vasoconstrictive properties.
• Profoundly stimulates alpha receptors of the sympathetic nervous

system
• Minimally stimulates beta receptors.
• Indicated for severe cardiogenic shock and haemodynamic

hypotension (B/P < 70 mmHg) that is refractory to other
management.
• Considered a ‘last resort’.

DOBUTAMINE
• DOBUTAMINE: a synthetic agent modelled on dopamine that
primarily stimulates myocardial beta 1 and smooth muscle
beta 2 receptors.
• Effects vary depending on dose.
• LOW DOSE: Alpha stimulation < Beta, therefore produces

increased myocardial contraction and mild vasodilatory
response = reduced afterload
• HIGH DOSE: causes increased noradrenaline production:

increased peripheral vascular resistance
ATROPINE
• ATROPINE: an anticholinergic agent that works by blocking
muscarinic receptor sites, leading to reduced
parasympathetic stimulation of target organs.
• Atropine counters “rest and digest” stimulation, therefore

increasing heart rate.
• Indicated in bradycardia caused by vagal stimulation or

cholinergic drug toxicity.
• May also be used as a secondary agent in asystole or PEA

cardiac arrest
QUESTION TIME…?
• List five cardiac effects of adrenaline.
• The activation of vasoprsessin-1 receptors causes what affects?
• Why is noradrenaline administered via large-bore IV infusion?
• Which vasoactive drug is a synthetic agent that primarily stimulates the

beta receptors?
• Why is it necessary to administer Adrenaline in continuous short

intervals?
• What are the indications for use of atropine?

Summary
• SHOCK: the inability of the circulation to adequately perfuse the tissues of
the body.
• PERFUSION: the ability of the body to adequately circulate blood and

provide oxygen to cells.
• HYPOPERFUSION: any malfunction that causes a decrease in cellular

oxygenation.
• To achieve adequate perfusion, three components of cardiovascular system

must work properly:
• Heart: must sufficiently pump fluid
• Vasculature: must maintain integrity and enable blood flow
• Lungs: must adequately on/off-load oxygen
Summary
• Preload: the amount of blood returning to the ventricles; it is the end-
diastolic volume (EDV).
• Afterload: the total resistance against which blood must be pumped.
• MAP = diastolic pressure + 1/3 pulse pressure
• Pulse Pressure (PP): represents the difference between systolic and

diastolic pressure, represents the tone of the arterial system.
• Healthy body can be viewed as a smooth-flowing fluid-delivery system

inside a “container” (the human body)
Summary
• The progression of shock in microcirculation follows a
sequence of stages related to:
• Changes in capillary perfusion
• Cellular necrosis
• There are four stages:

• Vasoconstriction
• Capillary and venule opening
• Disseminated intravascular coagulation
• Multiple organ failure
Summary
• An understanding of the capillary-cellular relationship in
shock allows for these broad categorisations:
• Compensated shock: there is some decreased blood flow

and perfusion to tissues
• Decompensated shock: compensatory mechanisms fail

and SBP can no longer be maintained.
• Irreversible shock: there is cellular ischaemia and necrosis

and subsequent organ failure.
Summary
• There are five general classifications of shock:
• Hypovolaemic
• Cardiogenic
• Neurogenic
• Anaphylactic
• Septic
• Every shock patient (apart from cardiogenic shock) requires a
volume expander as part of this process to ensure the ‘container’ is
full.
• CRYSTALLOID SOLUTIONS: are created by dissolving crystals such as
salts and sugars in water
• COLLOID SOLUTIONS: contain molecules (eg: proteins) that are too
large to pass through the capillary membrane.
Summary
• KEY PRINCIPLES OF SHOCK MANAGEMENT
• Establish and maintain open airway: administer high-concentration

O2,assist ventilations
• Control external bleeding
• Initiate IV fluid: two large-bore IV lines of volume-expanding fluid
• Maintain normal body temperature: patients in shock often are unable
to conserve body heat and can become hypothermic easily
• Position: In absence of spine or head injury and if hypovolaemia is
suspected, consider positioning patient in with legs raised
• Monitor: cardiac rhythm and O2 saturation
• Reassess: frequently reassess vital signs en-route
Summary
• In conjunction with fluid resuscitation, there are also
pharmacological means for maintaining perfusion and managing
shock.
• This is done by using vasoactive drugs to increase peripheral

vascular resistance or rate and quality of cardiac contraction.
• These drugs include:

• Adrenaline
• Vasopressin
• Noradrenaline
• Dobutamine
• Atropine

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Edith Cowan University

School of Medical Sciences

PST2235: Medical Studies for Paramedics 1

• We now have a more scientific and specific definition:

• SHOCK: the inability of the circulation to

• Whilst there may be one specific cause, the overall

• Therefore: shock can not be adequately defined by pulse

• A good Paramedic must take a ‘global’ approach and have

• HYPOPERFUSION: any malfunction that causes a

• When discussing shock, we are really discussing the

• Simply: Perfusion is everything!!

• Think: What does a well-perfused patient look like?

• Heart: must sufficiently pump fluid

• Vasculature: must maintain integrity and enable

• Lungs: must adequately on/off-load oxygen

TISSUE OXYGENATION - HEART

• It depends on the following:

• The formula used to determine cardiac output is:

Cardiac output (CO) = Heart rate (HR) × Stroke volume (SV)

• eg: CO = 80 (bpm) × 70 (ml) = 5600 ml/min

TISSUE OXYGENATION - HEART

• MEAN ARTERIAL PRESSURE

TISSUE OXYGENATION - HEART

• It is the ‘load’ that is given to the left ventricle before

• EDV has a direct effect on the stretch of the

TISSUE OXYGENATION - HEART

• It is the ‘load’ that the heart

• It is directly affected by total

TISSUE OXYGENATION - HEART

• It represents the average pressure of the vasculature system

• The formula used to determine MAP is:

MAP = diastolic pressure + 1/3 pulse pressure

• Note: Pulse Pressure= systolic minus diastolic.

• What is the formula for calculating cardiac output?

• What three factors determine cardiac output?

CAPILLARY - CELLULAR RELATIONSHIP IN SHOCK

• The progression of shock in microcirculation follows a

• There are four stages:

• This constriction helps to maintain systemic BP

• Due to the narrowing of the entrance to the microcirculation, the

• This leads to an increase in hydrostatic pressure in capillaries and

• Fluid is reabsorbed as it shifts from extravascular space: this is called

1. O2 and nutrient delivery to cells by capillaries

• This reduces the pressure on

• The vasoconstriction stage of shock must be treated by

CAPILLARY AND VENULE OPENING

• This results in some expansion of vascular space

• However, post-capillary sphincters will resist these

CAPILLARY AND VENULE OPENING

• Vascular space continues to expand as increasing hypoxaemia and

• Normal blood volume inadequate to fill the “container”

CAPILLARY AND VENULE OPENING

• As acidosis increases (pH falls), red blood cells begin to

• This stage of shock can easily progress further if fluid

DISSEMINATED INTRAVASCULAR COAGULATION

• Due to decreases in flow, blood begins to

DISSEMINATED INTRAVASCULAR COAGULATION

• As shock continues, lactic acid accumulates around cells

• Small areas of dead cells (micro-infarcts) develop in organs

MULTIPLE ORGAN FAILURE

• This depends on the underlying condition of the organ, however:

MULTIPLE ORGAN FAILURE

• BP falls dramatically (to levels of 60 mm Hg or less)

• Why do patients in the early stages of shock have