Haemodynamic Disorders

Question 1

Oedema: recall the aetiological classification of oedema, and explain the possible consequences of oedema at different sites

Answer 1

Oedema

• Abnormal increase in interstitial fluid.
• 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)
• Flow of interstitial fluid is governed by 1) hydrostatic and oncotic pressures and 2) endothelial permeability

Localised oedema

•Cerebral and pulmonary oedema

Causes:

1. Left heart failure
2. Inflammation
3. Venous hypertension
4. Lymphatic obstruction

Generalised oedema

•Fluid in serous cavities (>5L)

Causes:

1. Congestive heart failure
2. Hypoproteinaemia (low protein content)
3. Nutritional oedema

Causes of oedema

1) Increased hydrostatic pressure

Heart failure results in increase in hydrostatic pressure (generalised oedema)

2) Reduced plasma oncotic pressure ( 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)

3) Lymphatic obstruction

Localised oedema

Non pitting protein rich oedema

Obstruction by tumour, lymph node dissection, chronic inflammation

4) Sodium 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 (generalised oedema).

5) Inflammation

Loss of protein rich fluid locally

Heart Failure and Systemic oedema -> Reduced renal blood flowà activation of the renin-angiotensin system

Question 2

Define thrombosis and recall its causes and possible consequences

Answer 2

Thrombosis: abnormal blood clot formation in the circulatory system.

Virchow’s Triad:

1. Stasis
2. Vessel wall injury
3. Hypercoagulability

Thrombosis:

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

Blood 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
• Pale thrombus: Composed of fibrin and platelets
• Red thrombus: Composed of fibrin, platelets and red blood cells

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Thrombosis can happen ANYWHERE within the vasculature

Cardiac Thrombosis – stasis (e.g. due to atrial fibrillation) will result in the blood not moving fluidly leading to the formation of clots. These clots can embolise to cause, for example, strokes.

Arterial Thrombosis - e.g. myocardial infarction – usual due to vessel wall injury

• Occlusive thrombi composed of platelets, fibrin, red blood cells and leucocytes
• Mostly in coronary > cerebral > femoral arteries
• Most commonly superimposed on ruptured atherosclerotic plaques
• Atherosclerosis leads to endothelial injury and abnormal blood flow

Venous Thrombosis – e.g. DVT – classically due to a combination of stasis and hypercoagulabiliy

• Occlusive thrombi; due to sluggish blood flow
• Composed of red blood cells >platelets
• Can develop in healthy individuals with no risk factors
• Veins of lower extremities mostly commonly affected
• Venous thrombi have characteristic appearances with lines of Zahn (alternating layers of platelets and red blood cells)

Risk factor for venous thrombosis: age, obesity, malignancy, immobility, oral contraceptive pill

Four Fates of a Thrombus

1. Propagation: Accumulation of further platelets and fibrin in a semi-occlusive thrombus
2. Embolization: Thrombi can dislodge and travel through the circulation
3. Dissolution: Fibrinolysis in early thrombi; fibrinolytic agents ie t-PA
4. Organisation and Recanalisation:

• Older thrombi enveloped by fibroblasts, endothelial cells and smooth muscle cells
• Capillary channels develop within the thrombus

Question 3

Define embolism and infarction; recall the causes and possible consequences of each

Answer 3

Embolism: a detached intravascular solid, liquid or gaseous mass that is carried by the blood to a site distant from its point of origin

Pulmonary Embolism (PE)

•DEFINITION: an embolus that blocks a pulmonary artery

•Consequence depends on the SIZE of the embolus

Most emboli are fragments of dislodged thrombi

Rarer types of emboli:

1. Fat
2. Air
3. Amniotic fluid
4. Tumour

Thromboemboli can cause other problems including strokes, bowel infarctions and acute limb ischaemia.

Small emboli symptoms: shortness of breath, chest pain, dizziness

Large emboli: instantaneous death

Risk Factors for Deep Vein Thrombosis:

1. Immobility
2. Surgery ( orthopaedic/ pelvic)
3. Trauma
4. Contraceptive pill; oestrogen
5. Thrombophilia
6. Malignancy
7. Obesity
8. Past DVT
9. Increased age
10. Pregnancy

Infarction: tissue necrosis due to ischaemia

• Most commonly caused by thrombotic or embolic vascular occlusion, though other causes need to be excluded
• Red infarcts:
• Occur as a result of venous occlusion
• Occur in loose tissue; lungs
• Occur in organs with dual circulation ; lung, bowel
• Can reperfuse a site of previous arterial occlusion

•White infarct:

• Occurs as a result of arterial occlusion
• In dense/solid organs
• Infarcts can be subtle initially and become more prominent with time.
• They are wedge shaped.

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Myocardial infarction

Most commonly due to coronary artery occlusion

• Occlusive thrombus in coronary artery
• Acute plaque change/ rupture

Can also be due to :

• Coronary artery vasospasm
• Emboli (from left atrium-atrial fibrillation)
• Vasculitis
• Haematological abnormalities ( sickle cell disease)
• There is cardiomyocyte death

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Atherosclerosis

DEFINITION: chronic disease caused by the focal accumulation of lipids, fibrous tissue and smooth muscle cells in the tunica intima of an artery.

STABLE plaque:

• Less inflammation
• Thick fibrous cap
• Slow growing
• Low risk of rupture

UNSTABLE plaque:

• More inflammation
• Lipid-rich necrotic core
• Thin fibrous cap
• HIGH risk of rupture

Diseases caused by stable plaques:

• Stable angina
• Chronic limb ischaemia

Diseases caused thrombosis over an unstable plaque:

• Unstable angina
• Myocardial infarction
• Cerebral infarction

Acute limb ischaemia

Question 4

Haemorrhage: list causes and possible consequences of haemorrhage

Answer 4

Haemorrhage: extravasation of blood due to vessel rupture

Causes

• Trauma
• Intrinsic disease of the vessel/clotting

Consequences depend on:

• Size of haemorrhage
• Rate of bleeding

Manifestations of a Haemorrhage

• Hypovolaemic Shock
• Death
• Intracranial Haematoma -> Raised ICP
• Chronic Low Grade Haemorrhage -> Iron Deficiency Anaemia

Death doesn’t necessarily have to be due to a large haemorrhage, a small berry aneurysm rupturing in the brain can cause a fatal subarachnoid haemorrhage.

Haematoma = a localised mass of extravasated blood that is relatively or completely confined within an organ or tissue

Question 5

Shock: define shock and identify possible causes and mechanisms

Answer 5

Shock: a disease state in which tissue perfusion is insufficient to meet metabolic requirements:

• Characterised by HYPOtension
• Vulnerable Organs: brain, heart, lungs, bowel, kidneys

SHOCK:

Hypovolaemic = 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

Cardiogenic = due to impaired cardiac function (e.g. acute MI, cardiac tamponade)

•SV is reduced due to malfunctioning heart

Septic = 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.

Anaphylactic = 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.

Neurogenic = RARE – usually caused by traumatic damage to the sympathetic pathways.

• Results in a loss of vasomotor tone à widespread vasodilation à reduced SVR à reduced MAP
• Disruption of the sympathetic pathway may also impair the ability of the heart to compensate with tachycardia.