shock
DESCRIPTION
Shock. KVB. What is shock?. Shock is the clinical syndrome that results 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. - PowerPoint PPT PresentationTRANSCRIPT
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 Shock
• Hypovolemic• Cardiogenic• Neurogenic• Anaphylactic• Septic
Types of Shock
• Hypovolemic• Cardiogenic• Neurogenic• Anaphylactic• Septic
Distributive 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 Shock
TissueTissueperfusionperfusion
NaNa++ Pump PumpFunctionFunction
ATPATPsynthesissynthesis
AnaerobicAnaerobicmetabolismmetabolism
Cellular edemaCellular edema Vascular volumeVascular volume
Impaired cellularImpaired cellularmetabolismmetabolism
OO22 useuse
Intracellular NaIntracellular Na++
& water& water
Impaired Impaired glucose glucose
usageusage
Stimulation of Stimulation of clotting cascade & clotting cascade &
inflammatoryinflammatoryresponseresponse
Hypovolemic Shock
• 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 Shock
COCOR.A.S.R.A.S.ActivationActivation
DyspneaDyspnea
OO22
supplysupply
Volume/Volume/PreloadPreload
SVRSVR
PeripheralPeripheral& pulmonary& pulmonary
edemaedemaImpairedImpaired
myocardial functionmyocardial function
MyocardialMyocardialOO22 demand demand
CatecholamineCatecholamineReleaseRelease
Neurogenic Shock Sympathetic ToneSympathetic Tone
OrOr Parasympathetic ToneParasympathetic Tone
Vascular ToneVascular Tone
Massive VasodilationMassive Vasodilation
SVR & PreloadSVR & Preload Cardiac OutputCardiac Output
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 Shock
• 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-AldosteronePlasmaPlasmavolumevolume
[Na+][Na+]
KidneyKidney(juxtaglomerular(juxtaglomerular
apparatus)apparatus)Detected by
Releases
ReninRenin
AngiotensinogenAngiotensin I…Angiotensin I…
Converts
&/Or
Via ACE(AngiotensinConvertingEnzyme)
Angiotensin II…Angiotensin II…
Uncompenstated Shock
• Defense mechanisms begin to fail• Presentation
– Hypotension– Marked increase in heart rate– Rapid, thready pulse– Agitation, restlessness, confusion
Irreversible Shock
• 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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