Haemodynamic Disorders| Thrombosis, Infarction and Shock

Haemodynamic in biology is how blood flows through the cardiovascular system. Haemodynamics 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 healthy 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.

  • A haemodynamic disorder means that the perfusion is not normal and may cause injury, perhaps leading to organ failure
  • Hypercapnia is divided into active and passive. Active results from an increase in the arterial blood supply and passive from a decrease in the venous exit. The end 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, it also related to poor venous drainage, distension of the veins, venules, capillaries may be localised or systemic
  • Happens when the left ventricle fails, the lungs then become congested leading 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.

Oedema 


Oedema

  • Is a condition where there is an abnormal accumulation of fluid in the tissue spaces or the cavities of the body and can a result of congestion
  • In the 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

  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, perhaps a 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 the retention of sodium, therefore, there is retention in of water which causes increased blood volume, but the heart can’t cope. Consequently, 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, consequently an increase in hydrostatic pressure
  • This results in the loss of plasma into the interstitial space, a decrease in plasma volume and therefore a decrease in kidney perfusion

Lymphatic drainage

  • Oedema is usually localised and is the result of an inflammatory response, neoplasm or an obstruction. E.g. filariasis which is a worm infection that is transmitted by mosquitoes. 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

  • Following the failure of the left ventricle blood returning to the heart from the lungs id slowed leading to a backup 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

Thrombosis

Forming of the thrombus in an otherwise uninterrupted 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
  • If the vascular wall is intact, the endothelium isolates the blood from endothelial CT which 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 the release factors that cause more platelets to be aggregate and also 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
  • There are regulations in normal haemostasis that control coagulation. These are pro and anticoagulant factors.

 

The clotting process 


Thrombosis

Happens in the injured VS three influences

  1. Endothelial cell injury which can lead 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

Thrombosis

  • Slow blood flow does not allow dilution of the activated clotting factors
  • Thi 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 creates a predisposition to platelet an fibrin deposition on the vascular wall
  • Hypercoagulability is the alteration of the blood clotting mechanism which predisposes a person to thrombus formation. It is seen in some blood disorders and cancers

Thrombosis

  • 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 ca fragment to form a emboli
  • The frequent site of development is the left ventricle over an area of a heart attack damage, the auricles, the aorta, atherosclerosis in the large arteries and in aneurysms
  • Frequent sites for the development of the venous system are the dilated superficial varicose veins. The valves of the heart are particularly at risk when they affected by bacteria or fungi. Also the deep veins of the thighs, calves, and muscular veins resulting in a DVT

Thrombosis

  • Propagation to obstruct a blood vessel or brunch
  • Embolization part or whole
  • Removed by fibrinolytic action
  • Organization and recanalisation IE if the thrombus persists is organised by invading fibroblasts and capillaries
  • Sometimes they recanalised by capillary channels

Emboli

  • 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 possible sites of development are debris from atheroma and fat emboli. Emboli from the veins pass through the lungs and may, or ma does not cause infection
  • Emboli from the arterial develop in the legs, brain and the viscera and often cause infection
  • Pulmonary emboli; over 95% of the pulmonary emboli begin the deep veins of the legs breaking off from the BVT
  • Massive 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 infection
  • 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 may also resolve its self 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 familiar sources are debris from atheromas 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

  • This is next most common to thrombi- emboli and 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 dependant on the number and size of the fat globules

Air and Gas Emboli

  • This 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
  • The bone marrow it can cause ischaemic necrosis, particularly in the heads of the long bones which then need to be replaced

Infarction

  • Infarction is a localised of ischemic necrosis in an organ or tissue from the sudden blockage of its arterial supply. It is rarely  seen venous drainage but does happen in an organ that has no potential bypass channels such as the poverty of the testis
  • The obstruction causing infection is usually from thrombi or emboli

Shock

  • Due to the hyperperfusion of the cells and tissues because of an inadequate circulating blood volume
  • Maybe due
  • Hypovolaemia( bleeding) or fluid loss ( vomiting diarrhoea, large burns, not enough fluids
  • Reduced cardiac output (myocardial infarction, pulmonary embolus). Cardiogenic shock.

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 pool in the periphery, so there is a small hypovolemic shock in the end 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 Correction 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 decreasing of the renal output
  3. Irreversible – if the circulation and metabolism can 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.

 

References

Makkar, R. R., Fontana, G., Jilaihawi, H., Chakravarty, T., Kofoed, K. F., De Backer, O., … & Friedman, J. (2015). Possible subclinical leaflet thrombosis in bioprosthetic aortic valves. New England Journal of Medicine373(21), 2015-2024.
Mohamad, I. I., KEENSWIJK, W., BESOUW, M., Raes, A., & Vande Walle, J. (2015). Pathophysiology of nephrotic oedema in children. In 48th Annual scientific meeting of the European Society for Paediatric Nephrology (ESPN 2015) (Vol. 30, No. 9, pp. 1688-1688).
Perry, H., Lehmann, H., Mantovani, E., Thilaganathan, B., & Khalil, A. (2018). Correlation between central and uterine haemodynamics in hypertensive disorders of pregnancy. Ultrasound in Obstetrics & Gynecology.
Jardin, F., Gurdjian, F., Fouilladieu, J. L., Goudot, B., & Margairaz, A. (1979). Pulmonary and systemic haemodynamic disorders in the adult respiratory distress syndrome. Intensive care medicine5(3), 127-133.
Disclaimer: This the above article is purely for educational purposes and should not be used as a diagnostic tool.

 

If there are any factual inaccuracies, point them out in the comments section, and we will endeavour to fix them as soon as possible.

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