SHOCK Dr.Mohammed Sharique Ahmed Quadri Assistant Prof.Physiology Almaarefa College.

SHOCK

Dr.Mohammed Sharique Ahmed QuadriAssistant Prof.Physiology

Almaarefa College

2

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

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


• Heart fails to pump blood out

MAP = CO x SVR

HR Stroke Volume


Normal

MAP = CO x SVR

Cardiogenic

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


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)

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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

1

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Hypovolaemic shock

Fluid

Volume

(CVP/JVP)

Vascular

Diameter

(SVR)

Cardiac

Output

(SV x HR)

PRE-LOAD AFTER-LOAD

12

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Hypovolaemic shock

Fluid

Volume

(CVP/JVP)

Vascular

Diameter

(SVR)

Cardiac

Output

(SV x HR)

PRE-LOAD AFTER-LOAD

312

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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

21

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Cardiogenic shock

Fluid

Volume

(CVP/JVP)

Vascular

Diameter

(SVR)

Cardiac

Output

(SV x HR)

PRE-LOAD AFTER-LOAD

3 21

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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

40

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

SHOCK Dr.Mohammed Sharique Ahmed Quadri Assistant Prof.Physiology Almaarefa College.

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