The SHOCK Of Your Life

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The SHOCK Of Your Life !
Dr Hora Ejtehadi Dr Usama ALAlami
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Circulatory Shock
Pathophysiologic state in which tissue perfusion
is totally inadequate to meet the oxygen or
nutritional needs of the cells
Shock described as momentary pause in the act of
death
Shock is not a disease entity in itself, but a
response to some assault or injury the body has
experienced
Whatever the initiating event, the cause of death
in irreversible shock is microcirculatory failure
and the subsequent depression of cellular
metabolism
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Classification Of Shock
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Blood Volumes A Reminder
Contraction Systole, dilation diastole
At the end of diastole, the ventricle should
contain 135 ml of blood (EDV)
The amount of blood remaining in the ventricle at
the end of systole 65 ml (ESV)
The difference between these two volumes is the
stroke volume (SV) 70 ml/beat
Cardiac output Stroke volume x heart rate 5
litres/min
MAP CO x peripheral resistance
Monitoring of blood pressure is through
baroreceptors in the carotid sinus and aortic
arch. Send impulses to cardiovascular centre
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Frank-Starling Law Of The Heart
The heart normally pumps the blood returned to it
Therefore, the more blood that is returned to the
heart (venous return) the higher the EDV and
therefore the higher the stroke volume.
The extent of cardiac filling is referred to as
the preload
It is called the preload, because it is the work
load imposed on the heart before contraction even
begins
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Cardiogenic Shock
Pathophysiology
Disorders that can result in the acute
deterioration of cardiac function and can lead to
cardiogenic shock include
1) Myocardial infarction
2) Myecardial ischaemia
3) Sustained arrhythmia
Autopsy studies have shown that cardiogenic shock
is associated with loss of more than 40 of the
left ventricular myocardial function
Mortality rate from cardiogenic shock is high
(80)
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Symptoms
Clinical evidence of hypoperfusion (low cardiac
output)
Low urine output
Cool extremities, ashen and cyanotic
Systemic hypotension ultimately develops
(systolic pressure lt 90 mm Hg and MAP decreases
by 30 mm Hg)
Hypoperfusion propagates to tissues
Exertional dyspnea or dyspnea at rest,
palpitations and generalized anxiety
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Myocardial Pathology
Cardiogenic shock is marked by both systolic and
diastolic dysfunction
Patients who develop cardiogenic shock from acute
MI consistently have evidence of progressive
myocardial necrosis with infarct extension
The patients have multivessel coronary artery
disease with limited coronary blood flow reserve
Myocardial ischemia results in decreased
myocardial compliance
This increases left ventricular filling pressure
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Myocardial Pathology In Cardiogenic Shock
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Cellular Pathology
Anaerobic glycolysis
Intracellular acidosis (Why?)
Myocyte membrane pump fails
Sodium and calcium accumulate intracellularely ?
myocyte swelling
Lysosomes, nuclear membranes and mitochondria
breakdown
Oxidative stress and eventual apoptosis
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Reversible Myocardial Dysfunction
a) Myocardial stunning
b) Hibernating myocardium
Myocardial stunning represents postischemic
dysfunction that persists despite restoration of
normal blood flow
Hibernating myocardium is a state of persistently
impaired myocardial function at rest
Hibernating myocardium occurs because of severely
reduced coronary blood flow
Hibernating myocardium improves with
neovascularization
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Cardiovascular Mechanics Of Cardiogenic Shock
The left ventricle is able to eject less blood
volume per beat
The stroke volume is decreased due to weakened
ventricles
To compensate for the reduced stroke volume,
venous return is increased
The EDV increases
However, this creates a left ventricular
diastolic filling pressure
This results in backflow from the left ventricle
to the lungs
This causes pulmonary oedema (this explains
dyspnea)
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Due to low cardiac output (because of low stroke
volume), the tissues increase their oxygen
extraction
This contributes to substantial arterial oxygen
desaturation
Other Effects
Myocardial ischemia is further exacerbated by
compromised myocardial perfusion due to
hypotension and tachycardia
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Pancreatic Ischemia And Cardiogenic Shock
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Causes Of Cardiogenic Shock A Summary
1) Systolic Dysfunction
Myocardial contractility is abated
Systolic dysfunction mainly due to MI
Another cause for systolic dysfunction is severe
myocarditis
2) Diastolic Dysfunction
Increased left ventricular diastolic chamber
stiffness contributes to cardiogenic shock
Caused by ventricular hypertrophy
Detrimental hen systolic contractility is also
depressed
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3) Valvular Dysfunction
Acute mitral valve obstruction by means of a left
atrial thrombus results in decreased cardiac
output
Aortic valve regurgitations reduce forward flow f
blood and increase EDV and pressure ? aggravate
shock
4) Cardiac Arrhythmias
Bradycardia cause a reduction in cardiac output
thereby aggravating shock
5) Greatly Increased Afterload
Aortic or mitral stenosis
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Chest Radiography A Useful Technique For
Diagnosis Of Cardiogenic Shock
Most patients with cardiogenic shock exhibit
_at_ Interstitial pulmonary oedema
_at_ Cardiomegaly
_at_ Alveolar oedema
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Hypovolemic Shock
Diminished blood volume
Due to excessive bleeding (haemorrhage)
Loss of fluids derived from the plasma (e.g.
diarrhoea, excessive urinary loss and extensive
sweating)
Prominent in burns patients. Why?
a) Increase blood viscosity ? venous stasis
b) Increased capillary permeability (plasma
shifts from intravascular compartments to
interstitial space)
Plasma proteins lost ? limit fluid return to
capillary
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Neurogenic Shock
Generalized vasodilation caused by decreased
vasomotor tone
Blood volume remains normal
However, the capacity of the blood vessels is
increased
Venous return is therefore diminished
Cardiac output is reduced and so is tissue
perfusion
Reduction in vasomotor tone can occur at the
level of the vasomotor centre (neurogenic shock)
or at the level of the blood vessels (Vasogenic
shock)
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Neurogenic shock is enhanced by conditions in
which the vasomotor tone is reduced
_at_ Spinal anaesthesia
_at_ Direct damage to the vasomotor centre of the
medulla
_at_ Altered functions of the vasomotor centre in
response to low blood glucose levels (insulin
shock)
_at_ Actions of tranquilizer, narcotic or sedative
drugs
_at_ Spinal cord injury
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Septic Shock
Also known as endotoxic shock
Results from widespread, overwhelming infections

1/3 of cases caused by gram-positive organisms
such as streptococci, pneumococci and
staphylococci (50 mortality rate)
Gram-negative infections resulting in shock cause
higher mortality rates (75) (E.Coli infections)

Patients at risk are
_at_ Patients with indwelling catheters
_at_ Chronic debilitating disease
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