5.4.1 Circulatory Disturbances Flashcards
Oedema
Abnormal accumulation of fluid within interstitial tissues
What are the two types of oedema?
Non-inflammatory (low protein/cell) = transudate
Inflammatory (protein/cell rich) = exudate
What are the four pathogeneses of oedema?
- ↑ intravascular hydrostatic pressue
- ↓ plasma osmotic pressue (loss/lack of albumin)
- ↑ capillary permeability (inflammatory origin)
- ↓ lymphatic drainage (inflammation/compression)
What mechanism regulates blood pressure?
RAAS
Renin- Angiotensin- Aldosterone- System
How does increase hydrostatic pressure result in oedema?
↑ blood volume in microvasculature = ↑ hydrostatic pressure
Generalised (systemic) due to RHS/LHS heart failure
How does decreased osmotic pressure result in oedema?
↓ albumin = ↑ fluid filtration and ↓ absorption = generalised oedema
Hypoalbuminaemia - excessive loss or lack of production of albumin
How does increased vascular permeability result in oedema?
Stimuli = vasodilation = ↑ permeability
Proteins escape into interstitial fluid = ↑ osmotic pressure = fluid drawn into intersitial fluid = oedema
How does decreased lymphatic drainage result in oedema?
↓ drainage = ↑ fluid in interstitium - oedema
Describe the morphology of oedema
Gross: clear-yellow gelatinous fluid
Histo: pale eosinophilic homogenous fluid
What is hyperaemia
Active process of arterial dilation resulting in increased bloodflow = ↑ blood vol. in vessels
What is congestion?
Passive process of decreased blood outflow from a tissue = ↑ blood vol. in vessels
Pathology of hyperaemia
Occurs during early vascular response to inflammatory stimulus
Physiology of hyperaemia
- Occurs during ↑ O2 demand
- Dissipation of heat
- Digestion of food
Local vs generalised congestion
Local: obstruction/compression of venous outflow
Generalised: ↓ blood flow in heart/lungs = heart failure
What does chronic congestion cause?
Lack of bloodflow = tissue hypoxia = ischemia and fibrosis
Morphology of hyperaemia and congestion
Gross: H(bright red tissues), C(dark-red tissues)
Histo: dilation of blood vessels with RBCs
What is shock?
Circulatory dyshomeostasis due to ↓ CO or ↓ circulating blood vol. and ↑ peripheral vascular resistance
Three types of shock
Cardiogenic
- decreased stroke volume and output
Hypovolaemic
- decreased circulating BV
Blood maldistribution
- decreased effective circulating BV
Cardiogenic stroke
failure of the heart to adequately pump blood
due to:
- myocardial damage
- arrhythmia
- compression
- outflow obstruction
Hypovolaemic shock
reduced circulating blood
due to:
- haemorrhage
- fluid loss
Blood maldistribution shock
reduced effective circulating BV
due to:
- neural/cytokine induced vasodilation
- septic / anaphylactic / neurogenic shock
Three stages of shock
Nonpreogressive - reflex compensation mechanisms
Progressive - widespread tissue hypoxia
Irreversible - severe cellular / tissue damage
Nonprogressive phase of shock
- Baroreceptors detect ↓ BP → epinephrine → ↑CO + vasoconstriction = ↑ vascular pressure
- ↓ plasma vol. → ADH release (RASS)→ vasoconstriction →↑ peripheral resistance
Progressive phase of shock
- Intracellular aerobic resp. replaced by anaerobic resp. = excessive lactic acid = cellular and systemic acidosis
- metabolic acidosis ↓ tissue pH = blood pools
- ↓CO = endothelial cells risk hypoxic injury ∴ DIC
Irreversible stage of shock
- O2 and energy stores depleted
- vital organs fail
- DIC
