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

BP = CO X PVR

CO – Cardiac OutputPVR – Peripheral Vascular resistance

Tissue perfusion is driven by blood pressure

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Cardiac Output

CO = SV X HR

This means that

BP= SV X HR X PVRBlood Pressure = Stroke Volume X Heart Rate X Peripheral Vascular Resistance

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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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TYPES OF SHOCK

HYPOVOLEMIC

CARDIOGENIC

OBSTRUCTIVE

DISTRIBUTIVE

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DISTRIBUTIVE SHOCK

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Hypovolaemic

• Volume Loss

• Blood loss -HaemorrhagePlasma Loss -Burns ECF Loss - Vomiting & Diarrhoea

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Cardiogenic

• Pump FailureMay be due to – Inability of heart to Contract or– Inability of heart to pump blood

• Myocardial damage ( M.I)• Arrhythmias• Valvular damage

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Distributive

• Decreased Peripheral Vascular Resistance

• Septic Shock (inflammatory mediators)• Neurogenic Shock (loss of sympathetic control

on vascular tone)• ANAPHYLACTIC shock (presence of

vasodilator substances like histamine)

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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)

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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

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Distributive shock

Fluid

Volume

(CVP/JVP)

Vascular

Diameter

(SVR)

Cardiac

Output

(SV x HR)

PRE-LOAD AFTER-LOAD

32 1

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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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Compensatory reactions activated by hemorrhage.

– Vasoconstriction – Tachycardia – Venoconstriction – Tachypnea→increased thoracic pumping – Restlessness→increased skeletal muscle pumping (in some

cases) – Increased movement of interstitial fluid into capillaries– Increased secretion of norepinephrine and epinephrine– Increased secretion of vasopressin – Increased secretion of renin and aldosterone – Increased secretion of erythropoietin– Increased plasma protein synthesis

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Effect of hemorrhage on mean arterial pressure

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Sympathetic activation

• Tachycardia• Increased myocardial contractility (β1)• α-adrenergic receptor-mediated

vasoconstriction (β2-receptor-mediated vasodilatation in skeletal muscle, bronchodialatation )

• Overall increased COP and redistribution of flow: cardiac, cerebral, hepatic and muscle vascular beds

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Points to Ponder

• Goal is to maintain cerebral and cardiac perfusion• Vasoconstriction of splanchnic, and

renal blood flow• Compensatory mechanisms are not

effective over the long term and fails when shock state is prolonged.

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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.

‼ Absolute adrenocortical insufficiency due to bilateral adrenal hemorrhage or necrosis is rare(in septic shock) and that this may be associated with an impaired pressor response to norepinephrine(noradrenaline) and a worsen the prognosis.

cause of this phenomenon remain unclear.

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Inadequate tissue perfusion

Decreased oxygen supply

Anaerobic metabolism

Accumulation metabolic waste & lactate

Cellular failure (limited ATP produce)

Pathophysiology of shockcellular responses

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Understanding Shock• Cellular responses to decreased systemic oxygen

delivery• ATP depletion → Na+/ K+ pump dysfunction• Cellular edema – Due to accumulation of Na+

inside the cell• Hydrolysis of cellular membranes and cellular

death • Mitochondrial activity severely depressed and

lysosomal rupture may occur• systemic metabolic lactic acidosis that

overcomes the body’s compensatory mechanisms

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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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Harmful effects of inflammatory mediators • Damage to cell membranes• Impaired mitochondrial respiration• DNA strand breakage• Apoptosis, which may contribute to the organ damage• Vasodilatation • Maldistribution of regional blood flow• Abnormalities in the microcirculation:

– capillaries are obstructed– increased capillary permeability with interstitial

oedema.• and immune hypo-responsiveness associated with sepsis.• Coagulation disorders

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VICIOUS CYCLE Hypoperfusion

Cellular injury

Inflammatory mediators

Functional & structural changes in microvascular

circulation

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Global Tissue Hypoxia

• Endothelial inflammation and disruption• Inability of O2 delivery to meet demand• Result:

• Lactic acidosis• Cardiovascular insufficiency• Increased metabolic demands

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BREAK !

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CLINICAL FEATURES OF SHOCK

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Symptoms of Shock

• Anxiety /Nervousness

• Dizziness• Weakness• Faintness• Nausea & Vomiting• Thirst• Confusion• Decreased UO

• Hx of Trauma / other illness

• Vomiting & Diarrhoea

• Chest Pain• Fevers / Rigors• SOB

General Symptoms Specific Symptoms

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Signs of ShockPale

Cold & Clammy skin SweatingCyanosis

TachycardiaTachypnoea

Confused / AggiatatedUnconsciousHypotensiveStridor / SOB

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Hypovolaemic Shock

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Clinical Feature of Hypovolaemic shock

• Inadequate tissue perfusion:(a) Skin – Cold, Pale, Slate-grey, ‘Clammy’,

Slow capillary refill,

(b)Kidneys – Oliguria, Anuria

(c) Brain – Drowsiness, Confusion and Irritability.

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Clinical Feature of Hypovolaemic shock

• Increased sympathetic tone:(a) Tachycardia, narrowed pulse pressure, ‘weak’

or ‘thready’ pulse

(b) Sweating

(c) Blood pressure – may be maintained initially (despite up to a 25% reduction in circulating volume if the patient is young and fit),but later hypotension supervenes.

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Clinical Feature of Hypovolaemic shock

• Metabolic acidosis – compensatory tachypnoea.

• Extreme hypovolaemia may be associated with bradycardia.

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Cardiogenic Shock

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Clinical Feature of Cardiogenic Shock

• Sign & symptoms are consistent with those of heart failure

• Stagnation of blood flow & increase extraction of O2 from hemoglobin:– Lips, nail beds and skin become cyanotic

• Poor stroke volume :– Decrease in MAP & SBP– Near normal diastolic B.P due to vasoconstriction– Narrow pulse pressure

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Clinical Feature of Cardiogenic Shock

• Low renal perfusion pressure & aldosterone release:– Decrease urine output

• Elevated preload :– Rise in CVP and pulmonary capillary wedge

pressure• Poor cerebral perfusion:

– Alteration in cognition and consciousness

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Clinical Feature of Cardiogenic Shock

• Acute pulmonary oedema:– Tachypnoea, orthopnea, pulmonary crackles,

oxygen saturation < 90% on air, pulmonary oedema on CXR

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Obstructive Shock

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Clinical Feature of Obstructive Shock

• Elevated JVP and CVP• Pulsus paradoxus and muffled heart sounds in

cardiac ,tamponade.• Signs of pulmonary embolism

– Pulmonary oligaemia on X-ray– Dyspnoea– On ECG – P-Pulmonale, RAD

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Distributive Shock

Causes of Distributive Shock

• Decreased sympathetic activity: neurogenic– Brain or spine injury; anesthetics; emotion

• Vasodilator substances in blood– Type I hypersensitivity (anaphylactic shock)– Inflammatory response to infection (sepsis)

• Vessel damage from severe hypervolemia

Neurogenic Shock • Occurs after acute spinal cord injury or defect in vasomotor center in brainstem or sympathetic outflow to blood vessels

• Brain injury• Depressant action of drugs • General anesthesia (barbiturate)• Hypoxia/hypoglycemia

• Sympathetic outflow is disrupted leaving unopposed vagal tone

• Results in hypotension and bradycardia• Skin is dry and warm

Anaphylaxis

• Systemic response to the inflammatory mediators released in type I hypersensitivity

– Histamine, acetylcholine, kinins, leukotrienes, and prostaglandins all cause vasodilation

º What will happen when arterioles vasodilate throughout the body?

– Acetylcholine, kinins, leukotrienes, and prostaglandins all can cause bronchoconstriction

º What will happen when the bronchioles constrict?

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Clinical Feature of Anaphylactic shock

• Signs of profound vasodilatation:(a) Warm peripheries(b) Low blood pressure(c) Tachycardia.

• Erythema, urticaria, angio-oedema, pallor, cyanosis.• Bronchospasm, rhinitis.• Oedema of the face, pharynx and larynx.• Pulmonary oedema.• Hypovolaemia due to capillary leak.• Nausea, vomiting, abdominal cramps, diarrhea.

Angio-oedema

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Septic Shock

Sepsis or Systemic Inflammatory Response Syndrome (SIRS)

• Inflammatory mediators released into the circulation– Tumor necrosis factor

– Interleukins

– Prostaglandins

• Cause systemic signs of inflammation– Fever and increased respiration, respiratory alkalosis,

vasodilation, warm flushed skin

• Activate inflammatory pathways– Coagulation, complement

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Sepsis and Systemic Inflammatory Response • Infection: Invasion of normally sterile host tissue by

microorganisms• Bacteremia: Viable bacteria in blood• Systemic inflammatory response syndrome

(SIRS):The systemic inflammatory response to a variety of severe clinical insults. The response is manifested by two or more of the following:

■ Temperature > 38°C or < 36°C ■ Heart rate > 90 beats/min ■ Respiratory rate > 20 breaths/min or Paco2 < 4.3 kPa ■ White cell count > 12 × 109/L, < 4 × 109/L or > 10%

immature forms

• Sepsis: SIRS resulting from documented infection

Sepsis

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• Severe sepsis :Sepsis associated with organ dysfunction, hypoperfusion or hypotension. Hypoperfusion and perfusion abnormalities may include, but are not limited to, lactic acidosis, oliguria or an acute alteration in mental state, thrombocytopenia

• Septic shock: Severe sepsis with hypotension (systolic BP < 90 mmHg or a reduction of > 40 mmHg from baseline) in the absence of other causes for hypotension and despite adequate fluid resuscitation

Discussion:

• Why is septic shock called distributive?

• In the later phases of septic shock, blood volume decreases. What part of the inflammatory process explains this?

Sepsis or Systemic Inflammatory Response Syndrome (SIRS) (cont.)

Septic Shock

vasodilation

decreased peripheral resistance

decreased blood pressure

SEPTIC SHOCK40% mortality

Septic Shock

• Also called systemic inflammatory response syndrome (SIRS)

• Inflammatory mediators also increase the metabolic rate of tissues, so they need more oxygen

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Pattern of systemic inflammatory response

• CARS: compensatory anti-inflammatory

• response syndrome; • SIRS: systemic

inflammatory response

• syndrome.

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Clinical Feature of Septic shock ■ Pyrexia and rigors, or hypothermia (unusual).

■ Nausea, vomiting. ■ Vasodilatation, warm peripheries. ■ Bounding pulse. ■ Rapid capillary refill. ■ Hypotension (septic shock). ■ Other signs:

(a) Jaundice(b) Coma, stupor(c) Bleeding due to coagulopathy (e.g. from vascular puncture sites, GI tract and surgical wounds)(d) Rash and meningism

Shock Types & Physiology

Shock CVP/PCWP CO PVR

Hypovolumic

Septic

Cardiogenic

Neurogenic

Cardiac temponadeAnaphylactic

Shock Types & Physiology

Shock CVP/PCWP CO PVR

Hypovolemic ↓ ↓ ↑

Septic

Cardiogenic

Neurogenic

Cardiac temponadeAnaphylactic

Shock Types & Physiology

Shock CVP/PCWP CO PVR

Hypovolemic ↓ ↓ ↑

Septic ↓ ↑ ↓

Cardiogenic

Neurogenic

Cardiac temponadeAnaphylactic

Shock Types & Physiology

Shock CVP/PCWP CO PVR

Hypovolemic ↓ ↓ ↑

Septic ↓ ↑ ↓

Cardiogenic ↑ ↓ ↑

Neurogenic

Cardiac temponadeAnaphylactic

Shock Types & Physiology

Shock CVP/PCWP CO PVR

Hypovolemic ↓ ↓ ↑

Septic ↓ ↑ ↓

Cardiogenic ↑ ↓ ↑

Neurogenic ↓ ↓ ↓

Cardiac temponadeAnaphylactic

Shock Types & Physiology

Shock CVP/PCWP CO PVR

Hypovolemic ↓ ↓ ↑

Septic ↓ ↑ ↓

Cardiogenic ↑ ↓ ↑

Neurogenic ↓ ↓ ↓

Cardiac temponade

↑ ↓ ↑

Anaphylactic

Shock Types & Physiology

Shock CVP/PCWP CO PVR

Hypovolemic ↓ ↓ ↑

Septic ↓ ↑ ↓

Cardiogenic ↑ ↓ ↑

Neurogenic ↓ ↓ ↓

Cardiac temponade

↑ ↓ ↑

Anaphylactic ↓ ↑ ↓

Any questions?

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Refrences

• Essentials of pathophysiology by carol Mattson Porth, 3rd edition.

• Kumar & Clark's Clinical Medicine, 7th Edition