Shock. Objectives Vocab Define Shock Types of Shock Stages of Shock Treatment.
SHOCK
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Transcript of SHOCK
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SHOCK
Dr.Mohammed Sharique Ahmed QuadriAssistant Prof.Physiology
Almaarefa College
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WHAT IS SHOCK?
Inadequate Tissue
Perfusio
n
• 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
DISEASE STATES
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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
MAP = CO X PVR
CO – Cardiac OutputPVR – Peripheral Vascular resistance
Tissue perfusion is driven by mean arterial pressure
MAP
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Cardiac Output
CO = SV X HRThis means that
MAP= SV X HR X PVRBlood 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
Stroke Volume
• Volume of Blood pumped by the heart during 1 cycle
What affects Stroke volume?
Heart Muscle Damag
e
Blood Volume
MechanicalObstruction
Mechanical Obstruction
Rhythm Problems
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What makes up blood volume
Plasma
RBCs
WBCs
Platelets
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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
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Hypovolemic Shock: Pathophysiology
• Heart pumps well, but not enough blood volume to pump
MAP = CO x SVR
HR x Stroke volume
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Hypovolemic Shock:Pathophysiology
Normal
MAP = CO x SVR
Hypovolemic
MAP = ↓CO x SVR
MAP = ↓CO x ↑ SVR↓MAP = ↓↓CO x ↑ SVR
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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
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Cardiogenic Shock: Pathophysiology
• Heart fails to pump blood out
MAP = CO x SVR HR Stroke Volume
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Cardiogenic Shock: Pathophysiology
• Heart fails to pump blood out
MAP = CO x SVR
HR Stroke Volume
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Cardiogenic Shock: Pathophysiology
Normal
MAP = CO x SVR
Cardiogenic
MAP = ↓CO x SVR
MAP = ↓CO x ↑ SVR↓MAP = ↓↓CO x ↑ SVR
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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)
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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
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Obstructive Shock:Pathophysiology
Normal
MAP = CO x SVR
Obstructive
MAP = ↓CO x SVR
MAP = ↓CO x ↑ SVR↓MAP = ↓↓CO x ↑ SVR
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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
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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
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Distributive Shock:Pathophysiology
Normal
MAP = CO x SVR
Distributive
MAP = co x ↓ SVR
MAP = ↑co x ↓ SVR
↓MAP = ↑co x ↓↓ SVR
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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)
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PATHOPHYSIOLOGY OF SHOCK
• The manifestation of shock reflects both – The impaired perfusion of body tissue & – The body’s attempt to maintain tissue perfusion
(compensatory mechanism)
So the pathophysiology of shock can be explained as cellular hypoxia resulting from impaired tissue perfusion
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COMPENSATORY MECHANISMS
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Compensatory mechanism and shock
Fluid
Volume
(CVP/JVP)
Vascular
Diameter
(SVR)
Cardiac
Output
(SV x HR)
PRE-LOAD AFTER-LOAD
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Hypovolaemic shock
Fluid
Volume
(CVP/JVP)
Vascular
Diameter
(SVR)
Cardiac
Output
(SV x HR)
PRE-LOAD AFTER-LOAD
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Hypovolaemic shock
Fluid
Volume
(CVP/JVP)
Vascular
Diameter
(SVR)
Cardiac
Output
(SV x HR)
PRE-LOAD AFTER-LOAD
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Hypovolaemic shock
Fluid
Volume
(CVP/JVP)
Vascular
Diameter
(SVR)
Cardiac
Output
(SV x HR)
PRE-LOAD AFTER-LOAD
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Cardiogenic shock
Fluid
Volume
(CVP/JVP)
Vascular
Diameter
(SVR)
Cardiac
Output
(SV x HR)
PRE-LOAD AFTER-LOAD
1
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Cardiogenic shock
Fluid
Volume
(CVP/JVP)
Vascular
Diameter
(SVR)
Cardiac
Output
(SV x HR)
PRE-LOAD AFTER-LOAD
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Cardiogenic shock
Fluid
Volume
(CVP/JVP)
Vascular
Diameter
(SVR)
Cardiac
Output
(SV x HR)
PRE-LOAD AFTER-LOAD
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Distributive shock
Fluid
Volume
(CVP/JVP)
Vascular
Diameter
(SVR)
Cardiac
Output
(SV x HR)
PRE-LOAD AFTER-LOAD
1
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Distributive shock
Fluid
Volume
(CVP/JVP)
Vascular
Diameter
(SVR)
Cardiac
Output
(SV x HR)
PRE-LOAD AFTER-LOAD
2 1
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Distributive shock
Fluid
Volume
(CVP/JVP)
Vascular
Diameter
(SVR)
Cardiac
Output
(SV x HR)
PRE-LOAD AFTER-LOAD
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Type of Shock
Insult Physiologic Effect
Compensation
CompensationHeart Rate
CompensationContractility
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 well, but not enough blood volume to pump
↓CO BaroRc↑SVR
↑ ↑
Distributive Heart pumps well, but there is peripheral vasodilation
↓SVR ↑CO ↑
No Change - in neurogenic shock
↑
No Change - in neurogenic shock
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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 InflammatoryMediators
• 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 & releaseof potentially damaging ‘mediators’)
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Release of Pro- and Anti InflammatoryMediators (continued)
• Pro inflammatory Mediators:– Proteases– Toxic free radicals & other reactive oxygen species– Cytokines
• IL• TNF
– Platelet activating factor• Hypotension, Inc. vascular permeability, platelet
aggregation.
• Anti inflammatory mediators:– Interleukin 10 ( IL-10)
Are involved in leukocyte adhesion ,local inflammation, neutrophil activation, fever, lactic
acidosis, ventilation perfusion abnormalities
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Release of Pro- and Anti InflammatoryMediators (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
ReferenceKumar & Clark's Clinical Medicine, 7th Edition