Transcript CO (HR x Stroke Volume)

SHOCK
Dr.Mohammed Sharique Ahmed Quadri
Assistant Prof.Physiology
Almaarefa College
WHAT IS SHOCK?
• Shock is the term used to describe acute
circulatory failure with inadequate or
inappropriately distributed tissue perfusion
resulting in generalized cellular hypoxia
and/or an inability of the cells to utilize
oxygen.
SHOCK IS A SYNDROME THAT CAN OCCUR IN THE COURSE OF
MANY LIFE THREATENING TRAUMATIC CONDITIONS OR
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DISEASE STATES
Or it can be define simply as
A clinical state in which tissues do not receive
adequate blood flow and O2 to meet their
metabolic needs.
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Physiological Principles
Tissue perfusion is driven by mean arterial pressure
MAP
MAP = CO X PVR
CO – Cardiac Output
PVR – Peripheral Vascular resistance
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Cardiac Output
CO = SV X HR
This means that
MAP= SV X HR X PVR
Blood Pressure = Stroke Volume X Heart Rate X Peripheral Vascular Resistance
•
•
MAP= DP+ 1/3 PP and normal value for adult is between 60 and 110 mm Hg
Normal adult CO is about 5 L/ min& is equal for both ventricles
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Stroke Volume
• Volume of Blood pumped by the heart
during 1 cycle
What affects Stroke volume?
Blood
Volume
Mechanical
Obstruction
Rhythm Problems
Heart
Muscle
Damage
Stroke
Volume
Mechanical
Obstruction
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What makes up blood volume
Plasma
RBCs
Platelets
WBCs
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What Alters Blood Volume?
• Haemorrhage
• Plasma Loss
• Loss /Redistribution of Extracellular
Volume
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Heart Rate
• Heart rate increases as a
compensatory response to Shock
Heart rate too fast to allow adequate
refilling of heart between beats
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Peripheral Vascular Resistance
PVR regulated by
ARTERIOLAR tone.
Dilatation opens
Arteriovenous beds
& increases volume
of circulatory
system
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What Alters PVR?
• Circulating cytokines & Inflammatory
mediators (e.g. Histamine)
• Endotoxins
• Drugs (e.g. Nitrates)
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So tissue and cellular perfusion is
dependent on
• Adequate preload
• Functioning heart
• Intact blood vessels
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TYPES OF SHOCK
HYPOVOLEMIC
CARDIOGENIC
OBSTRUCTIVE
DISTRIBUTIVE
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Pathophysiology: Overview
• Tissue perfusion is determined by Mean Arterial Pressure
(MAP)
MAP = CO x SVR
Heart rate
Stroke Volume
Hypovolemic Shock: Pathophysiology
• Heart pumps well, but not enough blood volume to
pump
MAP = CO x SVR
HR x Stroke volume
Hypovolemic Shock:
Pathophysiology
Normal
MAP = CO x SVR
Hypovolemic
MAP = ↓CO x SVR
MAP = ↓CO x ↑ SVR
↓MAP
= ↓↓CO x ↑ SVR
Hypovolemic Shock: Causes
↓MAP = ↓ CO (HR x Stroke Volume) x ↑SVR
• Decreased Intravascular volume (Preload) leads to Decreased Stroke
Volume
– Hemorrhagic - trauma, GI bleed, AAA rupture, ectopic pregnancy
– Hypovolemic - burns, GI losses, dehydration, third spacing (e.g. pancreatitis,
bowel obstruction), Adesonian crisis, Diabetic Ketoacidosis
Cardiogenic Shock: Pathophysiology
• Heart fails to pump blood out
MAP = CO x SVR
HR Stroke Volume
Cardiogenic Shock: Pathophysiology
• Heart fails to pump blood out
MAP = CO x SVR
HR Stroke Volume
Cardiogenic Shock: Pathophysiology
Normal
MAP = CO x SVR
Cardiogenic
MAP = ↓CO x SVR
MAP = ↓CO x ↑ SVR
↓MAP
= ↓↓CO x ↑ SVR
Cardiogenic Shock: Causes
↓MAP = ↓ CO (HR x Stroke Volume) x ↑SVR
• Decreased Contractility (Myocardial Infarction, myocarditis,
cardiomypothy, Post resuscitation syndrome following cardiac arrest)
• Mechanical Dysfunction – (Papillary muscle rupture post-MI, Severe Aortic
Stenosis, rupture of ventricular aneurysms etc)
• Arrhythmia – (Heart block, ventricular tachycardia, SVT, atrial fibrillation
etc.)
• Cardiotoxicity (B blocker and Calcium Channel Blocker Overdose)
Obstructive Shock:
Pathophysiology
• Heart pumps well, but the output is decreased due
to an obstruction (in or out of the heart)
MAP = CO x SVR
HR x Stroke volume
Obstructive Shock:
Pathophysiology
Normal
MAP = CO x SVR
Obstructive
MAP = ↓CO x SVR
MAP = ↓CO x ↑ SVR
↓MAP
= ↓↓CO x ↑ SVR
Obstructive Shock: Causes
↓MAP = ↓ CO (HR x Stroke Volume) x ↑SVR
• Heart is working but there is a block to the outflow
–
–
–
–
Massive pulmonary embolism
Aortic dissection
Cardiac tamponade
Tension pneumothorax
• Obstruction of venous return to heart
– Vena cava syndrome - eg. neoplasms, granulomatous disease
– Sickle cell splenic sequestration
Distributive Shock:
Pathophysiology
• Heart pumps well, but there is peripheral
vasodilation due to loss of vessel tone
MAP = CO x SVR
HR x Stroke volume
Distributive Shock:
Pathophysiology
Normal
MAP = CO x SVR
Distributive
MAP = co x ↓ SVR
MAP = ↑co x ↓ SVR
↓MAP
=
↑co x
↓↓
SVR
Distributive Shock: Causes
↓MAP
= ↑CO (HR x SV) x ↓ SVR
• Loss of Vessel tone
– Inflammatory cascade
• Sepsis and Toxic Shock Syndrome
• Anaphylaxis
• Post resuscitation syndrome following cardiac arrest
– Decreased sympathetic nervous system function
• Neurogenic - C spine or upper thoracic cord injuries
– Toxins
• Due to cellular poisons -Carbon monoxide, methemoglobinemia, cyanide
• Drug overdose (a1 antagonists)
PATHOPHYSIOLOGY OF SHOCK
So the pathophysiology of shock can be explained as cellular
hypoxia resulting from impaired tissue perfusion
• The manifestation of shock reflects both
– The impaired perfusion of body tissue &
– The body’s attempt to maintain tissue perfusion
(compensatory mechanism)
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COMPENSATORY MECHANISMS
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Compensatory mechanism and shock
AFTER-LOAD
PRE-LOAD
Fluid
Cardiac
Vascular
Volume
Output
Diameter
(CVP/JVP)
(SV x HR)
(SVR)
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Hypovolaemic shock
AFTER-LOAD
PRE-LOAD
Fluid
Cardiac
Vascular
Volume
Output
Diameter
(CVP/JVP)
(SV x HR)
(SVR)
1
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Hypovolaemic shock
AFTER-LOAD
PRE-LOAD
Fluid
Cardiac
Vascular
Volume
Output
Diameter
(CVP/JVP)
(SV x HR)
(SVR)
1
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Hypovolaemic shock
AFTER-LOAD
PRE-LOAD
Fluid
Cardiac
Vascular
Volume
Output
Diameter
(CVP/JVP)
(SV x HR)
(SVR)
1
3
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Cardiogenic shock
AFTER-LOAD
PRE-LOAD
Fluid
Cardiac
Vascular
Volume
Output
Diameter
(CVP/JVP)
(SV x HR)
(SVR)
1
35
Cardiogenic shock
AFTER-LOAD
PRE-LOAD
Fluid
Cardiac
Vascular
Volume
Output
Diameter
(CVP/JVP)
(SV x HR)
(SVR)
1
2
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Cardiogenic shock
AFTER-LOAD
PRE-LOAD
Fluid
Cardiac
Vascular
Volume
Output
Diameter
(CVP/JVP)
(SV x HR)
(SVR)
3
1
2
37
Distributive shock
AFTER-LOAD
PRE-LOAD
Fluid
Cardiac
Vascular
Volume
Output
Diameter
(CVP/JVP)
(SV x HR)
(SVR)
1
38
Distributive shock
AFTER-LOAD
PRE-LOAD
Fluid
Cardiac
Vascular
Volume
Output
Diameter
(CVP/JVP)
(SV x HR)
(SVR)
2
1
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Distributive shock
AFTER-LOAD
PRE-LOAD
Fluid
Cardiac
Vascular
Volume
Output
Diameter
(CVP/JVP)
(SV x HR)
(SVR)
2
3
1
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Type of
Shock
Insult
Physio Compen Compensation
logic
sation
Heart Rate
Effect
Cardiogenic
Heart fails to
pump blood
out
↓CO
BaroRc
↑SVR
↑
↑
Obstructive
Heart pumps
well, but the
outflow is
obstructed
↓CO
BaroRc
↑SVR
↑
↑
Hemorrhagic
Heart pumps ↓CO
well, but not
enough blood
volume to
pump
BaroRc
↑SVR
↑
↑
Distributive
Heart pumps
well, but
there is
peripheral
vasodilation
↑CO
↑
↑
No Change in neurogenic
shock
No Change in neurogenic
shock
↓SVR
Compensation
Contractility
Sympatho-Adrenal Response to Shock
• Most immediate of compensatory mechanisms
are those of sympathetic nervous system and
renin angiotensin mechanism
• Sympathetic nervous system
• NE, epinephrine, and cortisol release
• Causes vasoconstriction, increase in HR, and
increase of cardiac contractility (cardiac
output)
• Renin-angiotensin axis
• Water and sodium conservation and
vasoconstriction
• Increase in blood volume and blood pressure
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Sympatho-Adrenal Response to Shock
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Neuroendocrine response
• Release of pituitary hormones such as
adrenocorticotrophic
hormone
(ACTH),
vasopressin(antidiuretic hormone, ADH).
• There is release of cortisol, which causes fluid
retention and antagonizes insulin.
• There is release of glucagon, which raises the
blood sugar level.
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Release of Pro- and Anti Inflammatory
Mediators
• Severe infection
(bacteraemia/endotoxaemia),
• Presence of large areas of
damaged tissue
(following trauma /extensive surgery)
• Prolonged episodes of hypoperfusion
Trigger an
exaggerated
inflammatory
response
(systemic
activation of
leucocytes &
release
of potentially
damaging
‘mediators’)
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Release of Pro- and Anti Inflammatory
Mediators (continued)
• Pro inflammatory Mediators:
– Proteases
– Toxic free radicals & other reactive oxygen species
– Cytokines
• IL
• TNF
Are involved in leukocyte adhesion ,local
inflammation, neutrophil activation, fever, lactic
acidosis, ventilation perfusion abnormalities
– Platelet activating factor
• Hypotension, Inc. vascular permeability, platelet
aggregation.
• Anti inflammatory mediators:
– Interleukin 10 ( IL-10)
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Release of Pro- and Anti Inflammatory
Mediators (continued)
• Although beneficial when targeted against
local areas of infection or necrotic tissue-dissemination of this ‘innate immune’
response can produce shock and widespread
tissue damage.
• Characteristically the initial episode of
overwhelming inflammation is followed by a
period of immune suppression--- increased
risk of developing secondary infections.
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TO BE CONTINUED TOMORROW
THANK YOU
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CLINICAL FEATURES OF SHOCK
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THANK YOU
Reference
Kumar & Clark's Clinical Medicine, 7th Edition
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