Shock

KVB

What is shock?

Shock is the clinical syndrome that Shock is the clinical syndrome that results from inadequate tissue perfusionresults from inadequate tissue perfusion

Classification of shock

Cardiogenic, due to heart failure

Hypovolemic (oligemic), due to fluid or blood loss

Distributive (hypotensive) owing to peripheral vasodilation

Types of ShockTypes of Shock

• Hypovolemic

• Cardiogenic

• Neurogenic

• Anaphylactic

• Septic

• Hypovolemic

• Cardiogenic

• Neurogenic

• Anaphylactic

• Septic

Types of ShockTypes of Shock

• Hypovolemic

• Cardiogenic

• Neurogenic

• Anaphylactic

• Septic

• Hypovolemic

• Cardiogenic

• Neurogenic

• Anaphylactic

• SepticDistributive shock

Common types of shock:

– Cardiogenic shock

– Hypovolemic shock

– Septic shock

Less common types of shock

• Neurogenic shock

• Anaphylactic shock

• Hypoadrenal shock

Common factor

• Circulatory collapse resulting from a disproportion between circulating blood volume & the vascular space that it has to fill.

• The ensuing tissue hypoxia or anoxia leads to multiple organ failure.

What happens with the perfusion deficit?

1. Insufficient delivery of oxygen & nutrients to cells and tissues.

2. Inadequate clearance of metabolites.

Outcomes of cellular hypoxia

1. Shift from aerobic to anaerobic metabolism.

2. This results in increased lactate production and later on, lactic acidosis.

• The metabolic & hemodynamic derangements are correctible at the outset & are associated with reversible cell injury.

• Persistence or worsening of the shock state leads to irreversible injury and death of cells and possibly , death of the patient.

Cellular Response to ShockCellular Response to Shock

TissueTissueperfusionperfusion

TissueTissueperfusionperfusion

NaNa++ Pump PumpFunctionFunction

NaNa++ Pump PumpFunctionFunction

ATPATPsynthesissynthesis

ATPATPsynthesissynthesis

AnaerobicAnaerobicmetabolismmetabolism

AnaerobicAnaerobicmetabolismmetabolism

Cellular edemaCellular edema Vascular volumeVascular volume

Cellular edemaCellular edema Vascular volumeVascular volume

Impaired cellularImpaired cellularmetabolismmetabolism

Impaired cellularImpaired cellularmetabolismmetabolism

OO22

useuse

OO22

useuse

Intracellular NaIntracellular Na++

& water& water

Intracellular NaIntracellular Na++

& water& water

Impaired Impaired glucose glucose

usageusage

Impaired Impaired glucose glucose

usageusage

Stimulation of Stimulation of clotting cascade & clotting cascade &

inflammatoryinflammatoryresponseresponse

Stimulation of Stimulation of clotting cascade & clotting cascade &

inflammatoryinflammatoryresponseresponse

Hypovolemic ShockHypovolemic Shock

• Decreased intravascular volume

• Causes:– Diarrhoea– Prolonged & excessive vomiting– Massive haemorrhage– Burns

• Decreased intravascular volume

• Causes:– Diarrhoea– Prolonged & excessive vomiting– Massive haemorrhage– Burns

Hypovolemic Shock

• Hemorrhage– external– internal

• GI tract

• hemothorax

• peritoneal or retroperitoneal space

• Loss of fluid into third space– burns– pancreatitis

Causes of cardiogenic shock1. Pump failure:

Ejection fraction < 20% Associated with myocardial

infarction Associated with Conduction

disturbances ( heart block or arrhythmias)

2. Obstructive heart failure Caused by massive pulmonary

emboli or valvular disease (Aortic stenosis)

Cardiogenic Shock

• Myocardial pump failure– myocardial infarction– myocardial rupture– cardiac arrhythmia

• Extrinsic compression– cardiac tamponade

• Outflow obstruction– pulmonary embolus

Cardiogenic ShockCardiogenic Shock

COCO COCOR.A.S.R.A.S.ActivationActivation

R.A.S.R.A.S.ActivationActivation

DyspneaDyspnea DyspneaDyspnea

OO22

supplysupply

OO22

supplysupply

Volume/Volume/PreloadPreload

Volume/Volume/PreloadPreload

SVRSVR SVRSVR

PeripheralPeripheral& pulmonary& pulmonary

edemaedema

PeripheralPeripheral& pulmonary& pulmonary

edemaedemaImpairedImpaired

myocardial functionmyocardial function

ImpairedImpairedmyocardial functionmyocardial function

MyocardialMyocardialOO22 demand demand

MyocardialMyocardialOO22 demand demand

CatecholamineCatecholamineReleaseRelease

CatecholamineCatecholamineReleaseRelease

Neurogenic ShockNeurogenic Shock

Sympathetic ToneSympathetic ToneOrOr

Parasympathetic ToneParasympathetic Tone

Sympathetic ToneSympathetic ToneOrOr

Parasympathetic ToneParasympathetic Tone

Vascular ToneVascular ToneVascular ToneVascular Tone

Massive VasodilationMassive VasodilationMassive VasodilationMassive Vasodilation

SVR & PreloadSVR & Preload SVR & PreloadSVR & Preload Cardiac OutputCardiac Output Cardiac OutputCardiac Output

TissueTissueperfusionperfusion

TissueTissueperfusionperfusion

Anaphylactic Shock

• Massive & systemic allergic reaction

• Large release of histamine

• Increases membrane permeability & vasodilation

Anaphylactic Shock

Caused by a hypersensitivity reaction to an allergen in a previously sensitised patient

Common allergens:

Common Features

• Angio-oedema• Bronchoconstriction• Vasodilatation and hypotension• Urticareal rash

Angio-oedema

Normal

Oedematous glottis

Septic Shock

• “Circulatory failure”

• Due to systemic infection

Septic Shock

• Leading cause of death in intensive care units

• Most cases (70%) are caused by gram negative bacteria (LPS-lipopolysaccharide)

• Also can occur with gram positive bacteria and fungal organisms

Effects of cytokine release

Effects Of Lipopolysaccharide (LPS) And Secondarily Induced Effector Molecules

MODS= Multiple organ dysfunction syndrome

Multiple Organ Dysfunction System

• Progressive dysfunction of two or more organ systems

• Caused by uncontrolled inflammatory response to injury or illness– Typically sepsis

Stages of ShockStages of Shock

• Compensated

• Uncompensated

• Irreversible

• Compensated

• Uncompensated

• Irreversible

STAGES OF SHOCK

• Initial stage (early compensation stage)

• Nonprogressive stage (compensatory)

• Progressive stage (intermediate)

• Refractory stage (irreversible)

Homeostatic Mechanisms in Shock• Baroreceptor reflexes and catecholamine release

– maintain cerebral and cardiac perfusion– decrease perfusion to gut, skin and kidneys

• Activation of renin-angiotensin system– angiotensin II constricts efferent arteriole of

glomerulus to maintain GFR– aldosterone promotes sodium retention

• Release of Arginine Vasopressin (ADH)– promotes renal conservation of water

Renin-Angiotensin-Aldosterone

PlasmaPlasmavolumevolume

PlasmaPlasmavolumevolume

[Na+][Na+] [Na+][Na+]

KidneyKidney(juxtaglomerular(juxtaglomerular

apparatus)apparatus)

KidneyKidney(juxtaglomerular(juxtaglomerular

apparatus)apparatus)Detected by

Releases

ReninReninReninRenin

AngiotensinogenAngiotensin I…Angiotensin I…Angiotensin I…Angiotensin I…

Converts

&/Or

Via ACE(AngiotensinConvertingEnzyme)

Angiotensin II…Angiotensin II…Angiotensin II…Angiotensin II…

Uncompenstated ShockUncompenstated Shock

• Defense mechanisms begin to fail

• Presentation– Hypotension– Marked increase in heart rate– Rapid, thready pulse– Agitation, restlessness, confusion

• Defense mechanisms begin to fail

• Presentation– Hypotension– Marked increase in heart rate– Rapid, thready pulse– Agitation, restlessness, confusion

Irreversible ShockIrreversible Shock

• Complete failure of compensatory mechanisms

• Death even in presence of resuscitation

• Complete failure of compensatory mechanisms

• Death even in presence of resuscitation

Symptoms of Shock

• Anxiety /Nervousness

• Dizziness• Weakness• Nausea &

Vomiting• Thirst• Confusion• Decreased Urine

Output

• History of Trauma / other illness

• Vomiting & Diarrhoea

• Chest Pain• Fevers / Rigors• Shortness of

breath (stridor)

General Symptoms Specific Symptoms

Signs of Shock• Pallor• Cold and clammy extremities• Sweating• Cyanosis• Tachypnoea• Tachycardia• Confusion & agitation• Stridor• Hypotension• Loss of consciousness

Features of compensated shock

• Tachycardia

• Skin pallor due to constriction of arterioles

• Reduced urine production

Features of decompenstaed but still reversible shock

• Hypotension

• Dyspnoea & tachypnoea

• Pulmonary oedema slowly develops, further worsening hypoxia

• Oliguria (urine volume<500ml/24hr)

• Acidosis due to anaerobic glycolysis

Features of irreversible shock

• Marked hypotension with extreme tachycardia (filiform pulse)

• Respiratory distress which is not responsive to oxygen therapy & assisted ventilation

• Loss of consciousness progressing to coma• Gastrointestinal bleeding• Anuria with elevated BUN & creatinine• Severe acidosis• Laboratory & clinical signs of DIC

Clinical Course

• Hypovolemic shock– If patient is young and healthy, most survive if

resuscitation restores perfusion

• Cardiogenic shock and septic shock– Up to 75% mortality even with best care

• Patients succumb with multi-organ failure– Tubular necrosis of kidneys– Ischemic enteropathy – Disseminated intravascular coagulation– Acute respiratory distress syndrome (septic shock)

Morphology of ShockHypoxic injury to multiple organs• Kidneys

– medulla and tubules most affected– acute tubular necrosis

• Gastrointestinal tract– mucosa most sensitive to hypoxia

• Brain• Heart

– subendocardial necrosis of myocardium

• Lungs– resistant to hypoxia but involved with septic shock

Kidney in shock:Coagulation necrosis of tubules

Renal Biopsy in DIC

Capillary loops of glomeruli occluded by fibrin thrombi.

H&E stain on left and MSB (Martius scarlet blue) for fibrin on the right

Myocardial necrosis(coagulation necrosis)

Adult respiratory syndrome (ARDS)

Synonyms:– Shock lung– Diffuse alveolar damage– Acute alveolar injury– Traumatic wet lungs

These are descriptive terms for a syndrome caused by diffuse alveolar capillary damage.

Clinically characterized by:

• Rapid onset of severe life-threatening respiratory insufficiency

• Cyanosis

• Severe arterial hypoxemia that is refractory to oxygen therapy

• Frequently progresses to extrapulmonary multisystem organ failure.

Some causes of ARDS:

• Shock

• Sepsis

• Extensive surface burns

• Massive fractures & other trauma

Morphology:

• In the acute edematous stage, the lungs are heavy, firm & boggy due to congestion, edema & inflammation.

Markedly congested & heavy lung

Microscopy

• Alveoli are lined by waxy hyaline membranes.

This is followed by:

• Proliferation of type II pneumocytes.

• However resolution does not usually occur.

• More commonly, there is organization of the fibrin exudate, with resultant intra-alveolar fibrosis.

• There is marked thickening of the alveolar septae.

• Mortality rate of ARDS is high (60%).

Approach to study:1. Definition of shock2. Classification of shock3. Causes of shock4. Pathogenesis of cardiac, neurogenic,

septic & anaphylactic shock5. Stages of shock including

compensatory mechanisms6. Clinical features of shock (at each

stage)7. Morphology of various organs &

tissues in shock

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