Shock Flashcards
What definitions can be used to describe shock?
- tissue perfusion inadequate for tissue’s metabolic requirement
- cellular and tissue hypoxia due to:
=> reduced O2 delivery, increased O2 consumption, inadequate O2 utilisation (or a combination)
What 3 components are required for normal tissue perfusion?
- Cardiac Function (heart as pump)
- Capacity of vascular bed (blood vessels
- Circulating blood volume
Why can normal perfusion not be measured and what is used as a surrogate marker?
- perfusion is different in every part of body
- BP is used instead (not perfect)
How is the mean arterial pressure calculated?
Mean Arterial Pressure =
C.O. (pump) x Systemic Vascular Resistance (vessels)
What are the main classifications of shock?
Hypovolaemic
Cardiogenic
Distributive - septic, anaphylactic
Obstructive - cardiac tamponade, tension pneumo, PE,
(Endocrine)
Explain the physiological problem in hypovolaemic shock
Loss of blood/plasma
=> not enough fluid in circuit
=> decreased systemic vascular resistance
=> decreased blood returning to heart (preload)
=> C.O. reduced
=> tissues cant be perfused
What would cause loss of plasma that may result in hypovolaemic shock?
Dehydration e.g. due to vomiting
extensive burns
Explain how pump failure results in cardiogenic shock
- decreased C.O. as pump not able to perfuse body
- usually caused by ischaemia from MI
- may also be due to cardiomyopathy/ valve defect
What can cause obstructive shock?
- mechanical obstruction => heart function is normal but pumping against something - PE, air embolus - Cardiac tamponade - Tension pneumothorax
What can cause distributive shock and what is the underlying pathophysiology of this subtype?
“hot” shock
- caused by sepsis, anaphylaxis, neuro etc
- Vasodilation occurs => circuit TOO BIG for circulating volume
=> SVR decreases, Preload decreases, C.O decreases
O2 extraction also impaired
What can precipitate endocrine shock?
- severe uncorrect hypothyroidism OR Addisonian Crisis
- causes decreased C.O and vasodilatation
How does the body attempt to compensate when in shock?
sympatho-adrenal response
=> aims to preserve CO and BP
- activates chemo and baroreceptors in vasomotor centre to increase sympathetics
How do neuroendocrine hormones help us to compensate when in shock?
Release of pituitary hormones – ACTH, ADH and endogenous opioids
=> Cortisol release – fluid retention, antagonises insulin
=> Glugagon release
Mixed pictures of shock are common (i.e. shock can be caused by multiple different things at the same time). TRUE/FALSE?
TRUE
these causes may come under different categories
Describe what happens during the inflammatory response in shocked patients?
- COMPLEMENT cascade (attracts leucocytes)
- CYTOKINES release – Interleukins, TNF-alpha
- Platelet activating factor – Increased vascular permeability, platelet aggregation
- Lysosomal enzymes – Myocardial depression, coronary vasoconstriction.
- Adhesion molecules – damage to vessel walls, leucocyte attraction
What haemodynamic changes can occur during shock?
- Vasodilatation/Constriction
- Maldistribution of blood flow
- Microcirculatory abnormalities – AV shunting, leaky capillaries
- Inappropriate coagulation (e.g. DIC)
- Reperfusion injuries
What is released in shock that causes blood vessels to lose their reactivity?
- Nitric oxide release (X1000) from endothelium => vessels fail to constrict
Myocardial dysfunction in shock occurs due to reduced coronary blood flow. TRUE/FALSE?
FALSE
- reversible biventricular systolic and diastolic dysfunction
- Cytokines have direct myocardial effect
- Beta-receptors down regulated
- Decreased cardiomyofilament calcium sensitivity
What are the main clinical features of shock?
CARDIOGENIC
- signs of myocardial failure
=> patient pale, clammy, cold peripheries
HYPOVOLAEMIC
- hypotension
OBSTRUCTIVE
- Raised JVP,
- Pulsus paradoxus
SEPTIC
- Pyrexia
- rapid cap refill
- hypotension
ANAPHYLACTIC
- vasodilatation => erythema
- bronchospasm
- oedema
Class 1 and 2 of hypovolaemic shock involves patients who are decompensated. TRUE/FALSE?
FALSE
- patients observations can be variable but often are compensating in this stage
e.g. the BP may be normal but this doesn’t tell you if all vessels are vasoconstricted in an attempt to maintain pressure
What should be monitored in patients with potential shock?
Examination – Pale, cold skin, prolonged capillary refill.
Urine output – Indicator of renal perfusion
Neurological – Disturbed consciousness a good indicator of cerebral hypoperfusion
Biochemical – Acidosis, lactate levels
How can pressures and cardiac output be measured in specialist centres?
Pulmonary capillary wedge pressures (surrogate for LA pressure)
C.O = Thermodilution with a PA catheter
What should be done whilst investigating for the cause of shock?
Establish wide bore IV access
resuscitate while investigating
What would be considered a minimal acceptable BP if the patient is alert?
70-80 mmHg
however be aware that patient is probably compensating and can’t be left like this for long
