Diseases Health

Haemodynamic Disorders, Thrombosis and Shock

Congestion is closely related to oedema, poor venous drainage, distension of the veins, venules and capillaries. It may be localised or systemic

Haemodynamic Disorders, Thrombosis and Shock

  • Haemodynamic in biology is how blood flows through the cardiovascular system
  • Haemodynamic is also related to cardiac output (perfusion pressure differences at various parts of the system and peripheral vascular resistance (the different perimeters combining to affect the blood flow in each organ)

Haemodynamic Disorders

  • Maintenance of a normal fluid balance is very important for survival. A large part of each cell is made of water, the surrounding component has water as does the plasma. So, an interruption to the blood supply or the fluid balance has a major impact on the functioning and the survival of the cells, tissue and the body as a whole.
  • Haemodynamic disorders mean that the perfusion is not normal and may cause injury, in the leading organ
  • Hypercapnia is divided into active and passive. Active results from an increase in the arterial blood supply and passive, happens as a decrease in the venous exit. The result is an increase in blood volume in the affected tissue.
  • Active hypercapnia is the dilation of the arterioles can be physiologically normal

Hypercapnia and Congestion

  • Congestion is closely related to oedema, poor venous drainage, distension of the veins, venules and capillaries. It may be localised or systemic
  • If the left ventricle fails, the lungs become congested leading to pulmonary oedema
  • If the right ventricle fails, systemic organs are affected, principally the liver followed by organs that drain into the liver in the flow on effect


  • Is one condition where there is an abnormal accumulation of fluid in the tissue spaces or the cavities of the body as a result of congestion
  • In an inflammatory response fluid accumulation is a normal part of the process where a protein-rich fluid leaks in the area of injury
  • This is different from the fluid of non-inflammatory oedema, which is a fluid that is low in protein because of improper functioning of the hydrostatic and osmotic forces between the blood vessels and the tissue
  • Intravascular hydrostatic and interstitial will move fluid out of the blood vessels. This is the opposite to interstitial fluid pressure and intravascular osmotic pressure which push/pull fluid in the blood vessels. The interstitial forces are small in both cases

Oedema happens when

  1. There is an increase in the intravascular pressure
  2. There is a decrease in the osmotic plasma pressure
  3. Blockage of lymph flow and retention of salt and water

Increased Intravascular Pressure

  • Poor venous outflow – often in lower limbs, as result of (DVT)
  • Increase venous pressure in congestive heart failure (right ventricle affected)

This causes

  • Reduced renal flow (because of reduced cardiac output which results in retention of sodium therefore there is a retention in of water which causes increased blood volume, but the heart can’t cope, therefore a further increase in venous pressure happens

Decreased pressure

  • Mainly caused by kidney disease (excrete albumin), this lowers the plasma osmotic pressure which reduces flow to the kidney; therefore, retain sodium and water
  • Liver disease e.g. cirrhosis of the liver increases portal hypertension, therefore an increase in hydrostatic pressure
  • This results in the loss of plasma into the interstitium, a decrease in plasma volume and therefore a decrease in kidney perfusion

Lymphatic Drainage

  • Oedema is usually localised and is a result of an inflammatory response, neoplasm or an obstruction. E.g. filariasis a worm infection that is transmitted by mosquitos. Causes fibrosis of the lymph nodes and channels of the inguinal area < 5% develop elephantiasis- which is another form of fluid build-up

Pulmonary oedema is an example of

  • Following the failure of the left ventricle blood returning to the heart from the lungs is slowed leading to a lack of blood in the lungs with the result being congestion
  • The pressure in the capillaries increase due to increased blood volume of congestion causing
  • Haemorrhages in the alveolar spaces
  • Increased hydrostatic pressure forcing fluid in the alveolar spaces (pulmonary oedema)
  • Increased fibrosis of interstitial in the lungs
  • Pulmonary hypertension as a result of increased venous pressure backing up into the arterial system this can further cause ventricular failure and systemic venous congestion


Forming of the thrombus in an otherwise an interrupted CV system, composed of RBC platelets, fibrin and other cells that may circulate within the blood. It will adhere to the endothelium. It may

  • Reduce or obstruct blood flow
  • Dislodge or fragment causing emboli
  • Form a thromboembolic

Normal haemostasis

Three key factors are involved in the making of a blood clot after the blood vessels have been cut

  1. Vascular wall injury, particularly the endothelium and the underlying CT
  2. Platelets
  3. Clotting factors
  4. If the vascular wall is intact the endothelium isolates the blood from subendothelial CT that is thrombogenic. Endothelial cells can be anticoagulants, antiplatelet or pro-coagulants

Normal Haemostasis

  1. When the endothelial is injured platelets are activated to form a clot
  2. Platelets then attach to the subendothelial collagen.
  3. Platelets release factors that cause more platelets to aggregate and cause vasoconstriction
  4. This causes the platelets to contract and form a platelet mass called a primary haemostatic plug
  5. Fibrin will be formed, and a definitive clot develops
  6. There are controls in the normal haemostasis that control coagulation these are pro and anticoagulant factors


Happens in the injured via three influences

  1. Endothelial cell injury which can by its self-cause thrombosis
  2. Abnormal flow and hypercoagulability of the blood

Atherosclerosis with Thrombosis

  • Abnormal flow. During normal blood flow the red cells are separated from the endothelium by the plasma. If there is turbulence such as at vascular bifurcation. It allows the platelets to contact the endothelium thereby activating the platelets to begin the clotting process


  • Slow blood flow does not allow dilution of the activated clotting factors
  • The slow blood flow slows down the inflow of clotting factor inhibitors
  • It also allows the build-up of aggregates of platelets in the area of the slow flow
  • This then causes endothelial cells injury, which in turn causes a predisposition to platelet a fibrin deposition on the vascular wall
  • Hypercoagulability is the alteration to the blood clotting mechanism which predisposes a person to thrombus formation. It is seen in some blood disorders and cancers


  • Morphology- a thrombus can form anywhere in the CV but the only place they to block the flow is the chambers of the heart and of the aorta because of the fast blood flow
  • In the remainder of the CV, they are usually occlusive. They are firmly anchored at the site they originate but can develop head or tails that can fragment to form a emboli
  • Artery frequent site of development is the left ventricle over an area of the heart attack damage, the auricles, the aorta, atherosclerosis in the large arteries and in aneurysms
  • Frequent sites for the development in the venous system are the dilated superficial varicose veins. The heart valves are particularly at risk when they are affected by bacteria or fungi. Also, the deep veins of the thighs, calves, and muscular veins resulting in a DVT


The thrombosis has several outcomes

  • Propagation to obstruct a blood vessel or brunch
  • Embolization part or whole
  • Removed by fibrinolytic action
  • The organisation and recanalization IE if the thrombus persist is organised by invading fibroblast and capillaries
  • Sometimes they recanalized be by capillary channels


  • Defined as an intravascular liquid or mass that is carried to a distant site from where it was formed, most of the emboli arise from thrombi other sites of development are debris from atheroma and fat emboli. Emboli from the veins pass through the lungs and may or may not cause infarction
  • Emboli from the arterial develop in the legs, brain and the viscera and often cause infarction
  • Pulmonary emboli; over 95% of the pulmonary emboli begin the deep veins of the legs breaking off from the DVT
  • Large emboli- 5% may lodge in the pulmonary artery or straddle the bifurcations of the pulmonary artery, they can cause instant death or cardiovascular collapse
  • Medium sized emboli will occlude medium-sized peripheral pulmonary branches usually causing infarction
  • Small emboli may be clinically silent or cause fleeting chest pain is the person is suffering from cardiac failure they may get small infarctions

Treatment of Pulmonary Emboli

  • Even without treatment there, we improved perfusion through the blocked area after the first day due to fibrinolysis and contraction of the thrombus and may even resolve itself in months. Treatment is usually with blood thinning agents

Arterial Emboli

  • Systemic embolism comes from thrombi in the heart after a heart attack
  • 5-10% come from auricles (associated with rheumatic heart disease)
  • Less common sources are debris from atheroma’s or thrombi from aortic aneurysms, infective endocarditis and prosthetic valves
  • They lodge in the lower limbs, brain and viscera and the upper limbs

Fat Embolism

  •  Thrombi- emboli consists of intravascular globules of fat
  • It is most often in people with fractures of large bones with fatty marrow. It is also seen in extensive trauma in fatty tissue. In rare cases, it is seen in diseases states such as diabetes mellitus or pancreatitis
  • The outcome is dependent on the number and size of the fat globules

Air and Gas Emboli

  • This is rare but does occur in underwater workers at high pressure of O2, N2 or He. The embolism happens when there is too rapid decompression and the excess gas release intravascular bubbles. These obstruct small vessels in the muscles and around joints causing bends
  • In the bone marrow it can cause ischaemic necrosis, particularly in the heads of the long bones which then need to be replaced


  • An infarction is a localised ischaemic necrosis in an organ or tissue from the sudden blockage of its arterial supply, it is rarely seen in venous drainage but does happen in an organ that has no potential bypass channels such as the ovary of the testis
  • The obstruction causing infarction are usually from thrombi or emboli


  • Due to the hyper perfusion of the cells a tissue because of an inadequate circulation blood volume. Can be due to Hypovolaemia (bleeding) or fluid loss (vomiting diarrhoea, large burns, not enough fluids
  • Reduced cardiac output (myocardial infarction, pulmonary embolus). Cardiogenic shock.


  • Less common are the anaphylactic shock, septic shock as a result of neurogenic and septic shock
  • Anaphylactic shock and neurogenic shock reduce circulating blood volume, causing blood to go into the periphery, so there is the small hypovolemic shock in the result
  • The consequences are metabolic, causing systemic cellular hypoxia leading to an increase in anaerobic metabolism and lactic acidosis all of which can lead to death

Clinical correlation of shock

  1. Compensated – mild hypotension tachycardia and pale cold clammy skin
  2. Decompensated – if low circulation persists the compensatory mechanism is overwhelmed- get lowered blood pressure, rapid pulse, breathing difficulties, acidosis and lowering of the renal output
  3. Irreversible – if the circulation and metabolism cannot be reversed the end result is coma and death. If the underlying cause of the shock is controlled with the fluid and electrolyte levels restored shock is reversible.


Mitchell, R. N. (2005). Hemodynamic disorders, thromboembolic disease, and shock. Robbins and Cotran Pathologic Basis of Disease. 7th ed. Philadelphia: Elsevier, 119-144.

Teboul, J. L., Saugel, B., Cecconi, M., De Backer, D., Hofer, C. K., Monnet, X., … & Squara, P. (2016). Less invasive hemodynamic monitoring in critically ill patients. Intensive care medicine42(9), 1350-1359.

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