Shock Flashcards
What is shock?
A state of cellular and tissue hypoxia due to either reduced oxygen delivery, increased oxygen consumption, inadequate oxygen utilisation, or a combination of these processes
Normal tissue perfusion relies on (3)
Cardiac Function
Capacity of vascular bed
Circulating blood volume
Surrogate markers for normal perfusion (4)
Blood pressure
Consciousness (Brain perfusion)
Urine output (Renal perfusion)
Lactate (General tissue perfusion)
Blood pressure and Perfusion
Mean Arterial Pressure (MAP) =
Cardiac Output (CO) x Systemic Vascular Resistance (SVR)
Why is perfusion important? (2)
Perfusion = oxygen delivery
DO2 = CO x [(1.34 x Hb x SaO2) + (PaO2 x 0.003)]
FOUR ways in which shock can be classified?
Hypovolaemic
Cardiogenic
Distributive
Obstructive
Hypovolaemic (6)
Acute haemorrhage
Also “Fluid deplete” states
=Severe dehydration
=Burns
Volume depletion – leading to reduced SVR
Reduced volume returning to heart – reduced pre-load and hence reduced CO.
Cardiogenic (7)
“Pump failure” – reduced CO
=Reduced contractility – “stroke volume”
=Reduced heart-rate
Primarily ischaemia induced myocardial dysfunction
Also: cardiomyopathies, valvular problems, dysrhthmias
If due to MI – suggests that >40% of LV is involved.
Unless correctable pathology (E.g. valvular), mortality >75%
Obstructive (7)
Mechanical obstruction to normal cardiac output in an otherwise normal heart
Direct obstruction to cardiac output = PE
=Air/Fat/Amniotic fluid-embolism
Restriction of cardiac filling = Tamponade
=Tension pneumothorax
Distributive (5)
“Hot” Shock
Septic, anaphylaxis, acute liver failure, spinal cord injuries
Due to disruption of normal vascular autoregulation, and profound vasodilatation.
Poor perfusion – despite increased cardiac output
Regional perfusion differences
Alteration of oxygen extraction
Endocrine shock (2)
Severe uncorrected hypothyroidism, Addisonian crisis – both reduced CO and vasodilation
Paradoxically – thyrotoxicosis
Sympatho-Adrenal Response
Pathways to preserve normal cardiac output, and hence blood pressure
Neuroendocrine response (4)
Release of pituitary hormones – Adrenocorticotrophic Hormone, Anti-diuretic hormone, endogenous opioids
Release of cortisol – fluid retention, antagonises insulin
Release of glucagon
Suggestion that some shock states (Sepsis), blunts the response to ACTH
Pathophysiology (4)
More complex than simply poor perfusion
Multiple aetiologies, same end pathway
Cascade of inflammatory mediators as a consequence of cellular ischaemia
Cause a vicious cycle of vasoconstriction and oedema – worsening cellular ischaemia – as well as direct cytotoxic damage.
The Inflammatory Response (4)
part of the pathological process (Sepsis), or consequence of (persisting hypoperfusion) and often both.
A protective reflex - Of benefit when targeted appropriately – but when disseminated, causes widespread harm.
Often followed by secondary immune suppression – leaving predisposition to secondary infection
Inflammatory Response (7)
Activation of complement cascade – attraction and activation of leucocytes
Cytokine release – Interleukins, TNF-alpha
Platelet activating factor – Increased vascular permeability, platelet aggregation
Lysosomal enzymes – Mycardial depression, coronary vasoconstriction.
Adhesion molecules – damage to vessel walls, further leucocyte attraction
Endothelium derived mediators – Nitric oxide
Imbalance between antioxidents and oxidents
Haemodynamic Changes (6)
Vascular abnormalities – Vasodilatation, or constriction
Maldistribution of blood flow
Microcirculatory abnormalities – AV shunting, “stop-flow” or “no-flow” capillary beds, failure of capillary recruitment, increased capillary permeability.
Inappropriate activation of coagulation system.
DIC
Reperfusion injuries
Loss of Vascular Reactivity (4)
The failure of vascular smooth muscle constriction
Nitric oxide – an important player in regulation of blood flow, coagulation, neural activity and immune function.
Produced in minute (picomolar) concentrations in endothelial and other cells by cNOS
Inflammation pathways activiate its inducible isoform iNOS in vessel smooth walls – leading to 1000 fold increase in NO production
Myocardial Dysfunction (5)
Reversible biventricular systolic & diastolic dysfunction
NOT because of reduced coronary blood flow
=Circulating cytokines with direct myocardial effect
=Beta-receptor downregulation
=Decreased cardiomyofilament calcium sensitivity
Clinical Features (12)
=hypotension
=signs myocardial failure
=raised JVP, pulus paradoxus
=pyrexia, vasodi, rapid cap refill, hypoten
=vasodi!, erythema, bronchospa ,oedema
Monitoring- Clinical (4)
Examination – Pale, cold skin, prolonged capillary refill.
Urine output – Sensitive indicator of renal perfusion
Neurological – Disturbed consciousness a good indicator of cerebral hypoperfusion
Biochemical – Acidosis, lactate levels
Monitoring- Pressures (4)
Blood pressure – either cuff, or invasive with arterial line
Central Venous Pressure – Value in itself rarely useful, can be useful to assess “fluid responsiveness”
Pulmonary Artery pressures- Rare
Pulmonary capillary wedge pressures (surrogate for LA pressure)- Rare
Monitoring – Cardiac Output (3)
Gold standard – Thermodilution with a PA catheter – rarely
Pulse contour analysis
Doppler ultrasonography
Management (4)
Prompt diagnosis, and treatment critical
ABC approach
Establishment of reliable, wide bore IV access and resuscitate while investigating
Identify – and treat – underlying cause
