Haemodynamic disorders (disorders of circulation) Flashcards
What is hyperaemia?
Arterial vasodilation resulting in more blood in blood vessels
What is congestion?
Venous outflow obstruction resulting in more blood in blood vessels
Types of hyperaemia
Physiological
- nervous impulse (blushing)
- functional demand -> muscles, during exercise
Pathological
- acute inflammation
Types of congestion
Localised
- deep vein thrombosis (DVT)
Generalised
- congestive heart failure
- heart fails as pump -> blood flow brought in by pulmonary veins undergo block
Congested organs
- result of congestive heart failure
- enlarged
- cyanotic
- firm and heavy
What is an oedema?
An excessive extravascular accumulation of fluid in interstitial tissues/body cavities
What are the pri causes of oedema?
Changes in Starling’s forces
- increased hydrostatic pressure
- reduced oncotic (osmotic) pressure
- increased endothelial permeability -> fluid leak out of vessel into tissue space
- lymphatic obstruction -> lymphatic sys drain fluid that can’t make it back into circulation
- Na and H2O retention
Classification of oedema
Localised
Generalised
Causes of localised oedema
Impaired venous drainage
- eg: venous occlusion due to thrombosis
Increased vascular permeability and hyperaemia
- eg: inflammation
Obstruction/destruction of lymphatics
- eg: filariasis, cancer
Why does impaired venous drainage lead to oedema?
Arterial flow can get in but venous flow cannot get out -> congestion -> increased hydrostatic pressure
Causes of generalised oedema
Cardiac cause
Renal cause
Hepatic cause
How does cardiac oedema happen?
Due to heart failure
- LHF -> congestion in pulmonary veins causing increase in hydrostatic pressure in pulmonary circulation -> fluid accumulation in lungs -> pulmonary oedema
- RHF -> systemic veins get congested -> congestion in dependent parts of body like lower limbs -> hydrostatic pressure in venous sys very high -> fluid leak out -> oedema
What is nephrotic syndrome?
Protein loss in urine due to glomerular disease
Pathogenesis of nephrotic syndrome
Reduced plasma oncotic pressure -> fluid lost into extravascular compartment by Starling’s forces -> oedema fluid accumulates in peritoneal cavity and gravity-dependent lower limbs
RAA sys activated -> kidney retains Na and H2O -> worsen oedema
What is the diff btw exudate vs transudate?
Exudate
- high protein content
- plasma and fibrinogen
- many inflammatory cells
Transudate
- low protein content
- albumin but no fibrinogen
- few inflammatory cells
Causes of haemorrhage
Traumatic
Spontaneous
- abnormal vessels
- platelets
- thrombocytopenia
- qualitative platelet defect
- coagulation factor deficiency
What is petechiae?
Small red dots
What is purpura?
Large red dots
What is petechiae usually due to?
Platelet deficiency
What is purpura usually due to?
Fragile blood vessels
Coagulation factor deficiency
What is ecchymoses?
Big bruises
What causes bleeding into joints?
Coagulation defects
How does the body initially respond to blood loss?
Maintenance of BP and flow by activating sympathetic nervous sys (heart beat faster and vessels vasoconstrict) / catecholamines (produced from adrenal medulla)
How does body compensate for vol loss?
Fluid retention via aldosterone, ADH
Redistribution of blood flow to vital organs
How does body respond to blood loss in the long term?
Replacement of red cells
- dependent on fning bone marrow
What are the consequences of unresolved blood loss?
Acute (severe)
- shock
Chronic
- anemia
What is shock?
A state of inadequate perfusion and tissue hypoxia due to inadequate cardiac output/effective circulating blood vol
What are the diff types of shock?
Hypovolemic shock - due to loss of volume
Cardiogenic shock - pump failure
Septic shock - due to generalised vasodilation
- aka distributive shock
What is the pathophysiology of septic shock?
Microbial antigens (i.e: lipopolysaccharide of endotoxins)
bind to endotoxin receptors of macrophages -> produce cytokines -> vasodilation -> decrease cardiac contractility -> endothelial cell activation and injury -> abnormal blood coagulation (DIVC)
Early signs of shock
Skin -> pale and cold
Kidneys -> low uring pdtn
Gut -> bowel stasis
Lung -> tachypnea
Liver -> fatty change
Brain -> reduced conscious level
Heart -> tachycardia
What happens as shock progresses?
Multi organ fialure
Cyanosis
Necrosis
Coma
Protocol for shock
Time sensitive
What are the vicious cycles of shock?
Heart: myocardial damage -> heart failure
Gut: mucosal damage -> loss of fluid, liberation of bacteria -> more vasodilation
Liver: impaired lactate catabolism -> acidosis -> impairs cardiovascular fn
Kidney: acute tubular necrosis -> renal failure -> acidosis -> impairs microcirculation
Lung: alveolar damage -> decreased oxygenation
What are the factors affecting the prognosis of shock?
Type and cause of shock
Prior condition of the pt/co-morbidities
Timeliness and effectiveness of treatment
Definition of thrombus
An intravascular blood clot formed during life
Definition of thrombosis
The process in which a thrombus is formed
What is Virchow’s triad?
3 key factors that increases thrombotic tendencies
Endothelial damage
- damage to endothelial wall promotes clot formation
Altered blood flow (stasis)
- slow blood flow reduces propensity of anti-coagulants to interact w/ coagulation factors
Hypercoagulability
- thrombophilia -> conditions that increase tendency for clot formation
Pathophysiology of venous thrombosis
Stasis -> build up of activated clotting factors -> deep vein thrombosis (DVT) (blood clot in the legs)
Where is arterial thrombosis most often seen?
In setting of atheromatous disease
What are some common clinical states that can lead to thrombosis?
Atrial fibrillation
Prosthetic cardiac valves
Post-operative/post-partum state
Prolonged bed rest/immobilisation
Disseminated cancer
Oral contraceptive (oestrogen)
Signs of local vascular occlusion
Local swelling
Pain
What is embolization?
Thrombus travels elsewhere and cause vascular occlusion
What is the clinical significance of thrombosis in arteries?
Thrombus in artery -> arterial occlusion -> ischemia
What are some possible outcomes of a thrombus?
Resolution/lysis
- body’s fibrinolysis get rid of blood clot naturally
Propagation
- extension of thrombus to form more complete occlusion of blood vessel
- possible to survive due to alternate blood flow
Organisation
- thrombus removed and replaced by granulation tissue and fibrosis
Recanalisation
- new blood vessels being formed -> restore a lot of blood flow
Embolism
- thrombus travel to another part of body
What is an embolus?
A detached intravascular solid, liquid or gaseous mass that is carried by the blood to a site distant from its point of origin
Types of thrombus and some eg
Solid
- detached thrombus
- tissue fragments
Liquid
- fat globules
- amniotic fluid
Gaseous
- air
- nitrogen
Septic
- infected material embolise
What are some effects of embolism?
Vascular occlusion -> necrosis of target organs -> death
Spread of infection (septic emboli)
Metastases
Where does pulmonary embolism come from?
Comes from venous thrombosis (deep veins of legs, pelvis)
Effects of pulmonary embolism
Sudden death
Pulmonary necrosis
Pulmonary hypertension
Why does pulmonary embolism cause sudden death?
Main trunk occlusion -> acute right heart failure
Is pulmonary necrosis acute or chronic?
Acute
How does pulmonary necrosis come about?
Due to arterial branch occlusion
Is pulmonary hypertension acute or chronic?
Chronic
How does pulmonary hypertension come about?
Widespread thromboembolic occlusion
Consequence of pulmonary hypertension
Right side heart failure
What are some special types of embolisms?
Fat
Air
Amniotic fluid
What is the source of a fat embolism?
Bone marrow
Causes of fat embolism
Traumatic fracture
Soft tissue/MSK injury
Pathogenesis of fat embolism
Cause vascular occlusion/damage
Are the effects of a fat embolism localised or widespread?
Widespread
Alternative name for air embolism
Decompression sickness
Signs of decompression sickness and why they happen
Chokes
- lungs -> breathless
Bends
- MSK -> pain
Staggers
- brain -> loss of balance
Pathogenesis for decompression sickness
Nitrogen moves from high pressure in the lungs into the blood (low pressure)
Swimming up too quickly does not give nitrogen enough time to leave the blood -> bubbles form -> air bubble ambolise -> DCS
Treatment for decompression sickness
Decompression chamber
How does amniotic fluid embolism occur?
Amniotic fluid containing dead skin cells of fetus gain access to uterine veins -> embolise
When does amniotic fluid embolism occur?
During delivery/abortion
What can amniotic fluid embolism progress to?
Acute right heart failure
What happens as amniotic fluid embolism progresses?
Material from amniotic fluid trigger coagulation cascade -> disseminated intravascular coagulation (DIVC)
Definition of infarction
Necrosis due to ischemia
- usually occlusion of artery, sometimes venous drainage
Types/colours of infarcts
White infarct
- common in solid organs
Red infarct
- superimposed w/ haemorrhage
Diff btw infarction due to arterial occlusion vs venous occlusion and eg for each
Arterial occlusion
- wedge shape
- eg: renal infarct
Venous occlusion
- haemorrhage
- eg: testicular torsion
What are the factors affecting development of an infarct?
Anatomy of arterial blood supply
- organs like liver/lungs more resistant as it has dual blood supply
Rate of development of vascular occlusion
- sudden -> body no chance to react -> more prone to ischemia and necrosis
- slow arterial supply -> body can react -> avert significant ischemia
Tissue vulnerability
- heart and lungs extremely vulnerable to ischemia
- tendons resistant to ischemia w/o undergoing necrosis
Presence of preexisting hypoxia
