SHOCK TERMINOLOGY DEFINITION TYPES OF SHOCK LISTED CLINICAL FEATURES OF SHOCK HYPOVOLAEMIC SHOCK CARDIOGENIC SHOCK SEPTIC SHOCK ANAPHYLACTIC SHOCK MISCELLANEOUS Brian Angus Pathology Department University of Newcastle upon Tyne Return to Cardiovascular Pathology Index Page

TERMINOLOGY Emotional/psychological Electrical Cardiovascular This presentation concerns acute circulatory failure: cardiovascular shock.

SHOCK TERMINOLOGY DEFINITION TYPES OF SHOCK LISTED CLINICAL FEATURES OF SHOCK HYPOVOLAEMIC SHOCK CARDIOGENIC SHOCK SEPTIC SHOCK ANAPHYLACTIC SHOCK MISCELLANEOUS

DEFINITION ACUTE CIRCULATORY FAILURE the clinical syndrome resulting from ACUTE CIRCULATORY FAILURE

SHOCK TERMINOLOGY DEFINITION TYPES OF SHOCK LISTED CLINICAL FEATURES OF SHOCK HYPOVOLAEMIC SHOCK CARDIOGENIC SHOCK SEPTIC SHOCK ANAPHYLACTIC SHOCK MISCELLANEOUS

TYPES OF SHOCK Cardiogenic Hypovolaemic Septic Anaphylactic Miscellaneous pancreatitis neurogenic blood transfusion

SHOCK TERMINOLOGY DEFINITION TYPES OF SHOCK LISTED CLINICAL FEATURES OF SHOCK HYPOVOLAEMIC SHOCK CARDIOGENIC SHOCK SEPTIC SHOCK ANAPHYLACTIC SHOCK MISCELLANEOUS

CLINICAL FEATURES OF SHOCK In acute circulatory failure the patient typically shows the following: Restless, confused Pale cold sweaty Peripheral cyanosis Rapid weak pulse Low blood pressure Drowsiness, coma

SHOCK a) TERMINOLOGY b) DEFINITION c) TYPES OF SHOCK LISTED d) CLINICAL FEATURES OF SHOCK e) HYPOVOLAEMIC SHOCK f) CARDIOGENIC SHOCK g) SEPTIC SHOCK h) ANAPHYLACTIC SHOCK i) MISCELLANEOUS

HYPOVOLAEMIC SHOCK AETIOLOGY Haemorrhage Burns (>10% surface) Vomiting/diarrhoea

HAEMORRHAGE: VOLUME EFFECTS Loss 10%: no effect Loss 25%: hypovolaemic symptoms 36hrs Loss 50%: coma. death.

LOSS OF BLOOD VOLUME EARLY COMPENSATORY CHANGES When blood is lost the body reacts specifically to preserve blood supply to the brain and heart. The adrenal gland secretes catecholamines which increase peripheral resistance (raising the blood pressure). The kidneys secrete renin which retains sodium and thus water by the renin angiotensin system

LOSS OF BLOOD VOLUME: MANAGEMENT 1 These early compensatory changes suffice if <25% blood volume lost. If>25% blood volume lost then transfusion is required as there is a risk of shock, dependent upon the age and health of the patient.

LOSS OF BLOOD VOLUME: MANAGEMENT 2 Transfusion is ideally done with crossmatched whole blood. Macromolecular solutions and saline can also be used.

LOSS OF BLOOD VOLUME MANAGEMENT 3 In assessing response to transfusion, measurement of central venous pressure (CVP) using a catheter inserted into the right side of the heart gives a better idea of the true circulatory status than simply measuring the blood pressure, which can be maintained by the compensatory mechanisms described until a critical situation is imminent.

HYPOVOLAEMIC SHOCK LATE EFFECTS 1 If blood volume is not restored, the following events take place, resulting in a critically ill patient: Circulation becomes sluggish because: artetioles relax and the vascular beds fill with subsequent departure of fluid into the extravascular compartment; this results in haemoconcentration. b) blood viscosity is raised because red cells form rouleaux, and the blood fibrinogen is raised.

HYPOVOLAEMIC SHOCK LATE EFFECTS 2 If blood volume is not restored, the following events take place, resulting in a critically ill patient: Damaged endothelium releases thromboplastins which trigger the coagulation cascade: this results in disseminated intravascular coagulation (DIC). Blood clotting factors are consumed and the patient therefore has a bleeding tendency.

HYPOVOLAEMIC SHOCK LATE EFFECTS 3 If blood volume is not restored, the following events take place, resulting in a critically ill patient: Lack of oxygen in the tissues results in metabolic acidosis: this depresses myocardial action. Damaged cells release potassium resulting in hyperkalaemia. Corticosteroid action (from the adrenals) results in hyperglycaemia.

HYPOVOLAEMIC SHOCK LATE EFFECTS 4 If blood volume is not restored, the following events take place, resulting in a critically ill patient: Widespread ischaemic damage occurs Brain: Neuronal necrosis Kidney: Acute tubular necrosis Heart: Subendocardial infarction

SHOCK a) TERMINOLOGY b) DEFINITION c) TYPES OF SHOCK LISTED d) CLINICAL FEATURES OF SHOCK e) HYPOVOLAEMIC SHOCK f) CARDIOGENIC SHOCK g) SEPTIC SHOCK h) ANAPHYLACTIC SHOCK i) MISCELLANEOUS

CARDIOGENIC SHOCK: CAUSES Myocardial infarction and its complications, for example ruptured papillary muscle, result in ACUTE PUMP FAILURE Mortality is high (at least 80%). The effects are similar to hypovolaemic shock, but of course management is different as there is no urgent requirement for fluid.

SHOCK a) TERMINOLOGY b) DEFINITION c) TYPES OF SHOCK LISTED d) CLINICAL FEATURES OF SHOCK e) HYPOVOLAEMIC SHOCK f) CARDIOGENIC SHOCK g) SEPTIC SHOCK h) ANAPHYLACTIC SHOCK i) MISCELLANEOUS

SEPTIC SHOCK: CAUSES Septic shock is caused by bacterial endotoxins or exotoxins in the blood . The toxins can be released, for example from bacteria in a focus of sepsis such as an abcess, or from bacterial growth in the flowing blood (septicaemia e.g. meningococcal)

EXOTOXIC AND ENDOTOXIC SHOCK

SEPTIC SHOCK: ENDOTOXIC and EXOTOXIC The diagram shows production of exotoxins by bacteria which remain intact (left). This contrasts with endotoxic shock where the whole bacteria break up and cell wall lipopolysaccarides activate the complement and coagulation cascades. In practice endotoxic and septic shock are often used synonymously.

SEPTIC SHOCK ENDOTOXIC: AETIOLOGY GRAM NEGATIVE ENDOTOXINS CELL WALL LIPOPOLYSACCARIDES E coli Proteus Klebsiella Bacteroides Pseudomonas (burns) Meningococci

SEPTIC SHOCK EXOTOXIC: AETIOLOGY GRAM POSITIVE EXOTOXINS Much rarer than endotoxic shock Example of cause: Staph aureus skin infection TOXIC SHOCK SYNDROME Straph aureus in tampons

SEPTIC SHOCK AETIOLOGY: SOURCES Infected burns Septicaemia Localised infections Instrumentation e.g. Urogenital Immunosuppression

SEPTIC SHOCK MECHANISM The toxins from bacteria damage endothelium. Nitric oxide (NO) is released which causes vasodilatation. Unlike hypovolaemic shock there is no vasoconstriction phase. However, as with late phase hypovolaemic shock, endothelial damage results in DIC as previously explained.

SEPTIC SHOCK EXAMPLE This is the haemorrhagic rash of meningococcal septicaemia. Prompt treatment can prevent the condition on the next slide:

SEPTIC SHOCK: EXAMPLE The brain is covered in purulent exudate: this is meningococcal meningitis University of Newcastle upon Tyne

SHOCK a) TERMINOLOGY b) DEFINITION c) TYPES OF SHOCK LISTED d) CLINICAL FEATURES OF SHOCK e) HYPOVOLAEMIC SHOCK f) CARDIOGENIC SHOCK g) SEPTIC SHOCK h) ANAPHYLACTIC SHOCK i) MISCELLANEOUS

ANAPHYLACTIC SHOCK: AETIOLOGY Histamine release from blood basophils Drugs e.g. penicillin Stings Foods e.g. Shellfish, Peanuts Vasodilatation - blood pressure drops

ANAPHYLACTIC SHOCK: MECHANISM Antigen, for example wasp venom accesses specific IgE on blood basophils. IgE dimerises at the cell surface and the basophil releases histamine by degranulation: vasodilatation causes the blood pressure to drop. Clinical features of shock develop rapidly.

ANAPHYLACTIC SHOCK: MECHANISM

ANAPHYLACTIC SHOCK: TREATMENT Adrenaline and hydrocortisone are given in the acute phase. The patient may recover without further specific treatment. If not, full support in an intensive care unit will be required.

SHOCK a) TERMINOLOGY b) DEFINITION c) TYPES OF SHOCK LISTED d) CLINICAL FEATURES OF SHOCK e) HYPOVOLAEMIC SHOCK f) CARDIOGENIC SHOCK g) SEPTIC SHOCK h) ANAPHYLACTIC SHOCK i) MISCELLANEOUS

MISCELLANEOUS CAUSES OF SHOCK Neurogenic : e.g. severe head injury Pancreatitis: enzymes damage endothelium Blood transfusion: incompatible

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