Heamodynamic disorders Flashcards
Define Oedema
An abnormal increase in interstitial fluid.
What three forces determine the movement of fluid between blood vessels and the interstitial space, and what is the normal condition?
Capillary hydrostatic pressure: pushing OUT of vessel
Tissue hydrostatic pressure: pushing IN to vessel
Plasma oncotic pressure: pulling IN to vessel. Pressure exerted by plasma protein
-Normally plasma oncotic pressure is greater than hydrostatic pressure in the pulmonary capillaries
Opposing forces ; hydrostatic pressure and plasma oncotic pressure keep interstitial fluid in balance in the microcirculation.
Fluid leaves the circulation at the arterial end ( hydrostatic pressure> oncotic pressure)
Fluid enters the circulation at the venous end ( oncotic pressure > hydrostatic pressure)
What are the 5 broad causes of oedema?
-Increased capillary hydrostatic pressure: Heart failure results in increase in hydrostatic pressure (generalised oedema)
-Decreased plasma oncotic pressure (e.g. reduced albumin)
Plasma oncotic pressure is governed by [albumin]
When [albumin] <25g/L fluid leaves the microcirculation
Cause of generalised oedema
Loss of protein ( nephrotic syndrome, protein loss enteropathy)
-Inflammation : increases vascular permeability, facilitates movement of fluid into the interstitum. Loss of protein rich fluid locally
-Lymphatic Obstruction; leads to bluid up of fluid. Localised oedema
Non pitting protein rich oedema
Obstruction by tumour, lymph node dissection, chronic inflammation
-Salt and water retention: Reduced cardiac output ( volume of blood pumped out of the heart per unit time) stimulates the renin-angiotensin system which leads to sodium retention + water (generalised oedema).
what are the types of oedema and the subcatogeries with the causes
Localised oedema
Cerebral and pulmonary oedema Causes: -Left heart failure -Inflammation -Venous hypertension -Lymphatic obstruction
Generalised oedema Fluid in serous cavities (>5L) Causes: Congestive heart failure Hypoproteinaemia (low protein content) Nutritional oedema
What are the fates of thrombi?
Propagation– thrombus accumulates fibrin and grows
Embolisation– thrombus dislodges and moves somewhere else
Dissolution– thrombus is dissolved by fibrinolytics
Organisation and Recanalisation– as a result of the thrombus, there is inflammation.
Thrombus becomes fibrotic and remodels. Lumen appears again allowing blood flow.
When do thrombosis come to clinical attention
- either obstruct arteries or veins
2. when they embolise
what is pale and red thrombus
Pale thrombus:
Composed of fibrin and platelets
Red thrombus:
Composed of fibrin, platelets and red blood cells
define shock
What are the types of shock?
a disease state in which tissue perfusion is insufficient to meet metabolic requirements. Low blood pressure
-Hypovolaemic shock: due to loss of intravascular volume (e.g. trauma, haemorrhage)
This leads to reduced cardiac output, and, consequently, reduced mean arterial pressure
The body tries to compensate by increasing heart rate.
-Cardogenic shock: due to impaired cardiac function (e.g. acute MI, cardiac tamponade)
SV is reduced due to malfunctioning heart
-Anaphylactic shock: IgE mediated hypersensitivity reaction results in widespread vasodilation and increased vascular permeability (leading to increased fluid leakage into the tissues).
Leads to reduced systemic vascular resistance and, hence, reduced mean arterial pressure.
-septic shock: a severe inflammatory response to bacteria in the blood leads to widespread vasodilation and leakage of fluid into the interstitium.
This leads to reduced systemic vascular resistance and, therefore, reduced mean arterial pressure.
-neurogenic shock: RARE – usually caused by traumatic damage to the sympathetic pathways.
Results in a loss of vasomotor tone widespread vasodilation reduced SVR reduced MAP
Disruption of the sympathetic pathway may also impair the ability of the heart to compensate with tachycardia.
What is a common cause of pulmonary oedema?
what are some consequences as a result
Caused: raised capillary hydrostatic pressure in the pulmonary capillary bed due to pulmonary venous congestion.
Cause: Left Ventricular Failure – build up of pressure in left atrium leading to back pressure into the capillaries – this pushes water into the interstitial space. Fluid accumulates in the interstitial space and then spills over into the alveolar spaces.This is cardiogenic pulmonary oedema.
Consequences include breathlessness and susceptibility to pneumonia.
What is non-cardiogenic pulmonary oedema and what is the main symptom?
Caused by increased permeability
Known as ARDS – Acute Respiratory Distress Syndrome
Often caused by Sepsis, Shock and Trauma
Main symptom: Dysponoea (breathlessness), but it is worse when lying down (orthopnoea).
Fluid in the alveolar spaces predisposes to bacterial infection in the lung (pneumonia
What are the four types of cerebral oedema?
- Vasogenic – physical breakdown of the blood-brain barrier – commonly due to trauma or tumours
- Interstitial – breakdown of CSF(Cerebrospinal Fluid Barrier) -brain barrier – commonly due to obstruction of the flow of CSF, which causes build up of CSF in the brain(Obstructive Hydrocephalus) .CSF moves into the interstitial space.
- Cytotoxic – derangement of the sodium-potassium pumps leads to a build up of intracellular sodium causing intracellular oedema, causing water to be taken up (common with ischaemic strokes)
- Osmotic – decrease in plasma osmolality – commonly caused by Syndrome of inappropriate ADH secretion (SIADH) that is commonly caused by small cell lung carcinoma. ADH is released, more water reabsorbed, causing decrease in plasma osmolality.
What are the possible serious consequences of cerebral oedema?
Rise in intracranial pressure, which could cause brain herniation (squeezing of the brain across a structure within the skull) and death.
Leads to confusion, nausea, and vomiting.
What are causes of generalised oedema and what is the consequence as a result?
Generalized oedema causes pitting peripheral oedema, pleural effusions and ascites.
The pathogenesis of generalized oedema is complex and multifactorial.
A key factor is thought to be activation of the renin-angiotensinaldosterone system which stimulates renal sodium retention. Common causes of generalized oedema include left ventricular failure, hepatic failure and nephrotic syndrome.
What is a consequence of oedema in a peripheral setting and the effects of patients on generalised oedema?
Impaired wound healing and patients with generalised oedema are more likely to get cellulitis (Cellulitis is a common bacterial skin infection.)
What is thrombosis
What are the three main factors affecting thrombus formation and what is this known as ?
Abnormal blood clot formation in the circulatory system.
Can develop in veins and arteries and heart Causes: Endothelial injury Stasis or turbulent blood flow Blood hypercoagulability 1 +2 +3= Virchow’s triad
Hypercoagulability:
Blood disorder that leads to thrombi formation
Can be primary or secondary
Primary; Factor V mutation, Protein C deficiency
Secondary; Multifactorial, obesity, cancer, stasis, advancing age, use of oral contraceptive pill
Endothelial injury- Endothelial injury leads to platelet activation
Arteries have high rates of blood flow and hence are under high shear stress; this leads to endothelial injury
Stasis or turbulent blood flow:
Stasis and turbulent blood flow leads to endothelial injury
Stasis; disruption of laminar blood flow and development of venous thrombi
Turbulent blood; endothelial injury and formation of local pockets of stasis
Turbulent blood ;arterial and cardiac thrombi
What is cardiac thrombosis caused by and what is an important complication?
Stasis is the main way that thromboses form – e.g. atrial fibrillation
Left artrial thrombosis: related to artrial fibrillation
Left ventricular thrombosis: related to prior myocardial infarction
Complication – systemic embolisation
