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Blood pressure in the blood vessels

Blood pressure in the blood vessels


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Why do the capillaries have a lower blood pressure than the arteries even though the capillaries lumen is much narrower. Wouldn't the narrowness of the blood vessel increase the pressure? Also the arterioles have an even larger lumen than the arteries so shouldn't the capillaries have a larger blood pressure than them as well?


Answer: You are right that if you had one big pipe that was getting progressively narrower, the pressure in that pipe would increase. In the vascular system, you have one big pipe emptying into exponentially more small pipes. The total lumenal diameter of the small pipes is actually greater than the single big pipe.

Even though each individual capillary has a smaller lumenal diameter than each artery, the sum lumenal diameter of all of the capillaries is much greater. This is because there are way more capillaries than there are arteries.

More detail: The following image plots total cross-sectional area and pressure in the pipe against the level of the circulatory system. The sum cross-sectional area of the vessels is highest in the capillaries, simply because there are so many capillaries. You can see the pressure decreases accordingly.


Lab: Measuring Blood Pressure

1. Deflate the air bladder of the cuff and place it around the upper arm so it fits snugly. If you’re right handed, you should hold the bulb/pump in your left hand to inflate the cuff. Hold it in the palm so your fingers can easily reach the valve at the top to open and close the outlet to the air bladder.

2. Put the head of the stethoscope just under the edge of the cuff, a little above the crease of the person’s elbow.

3. Inflate the cuff with brisk squeezes of the bulb. Watch the pressure gauge as you do it, you should go to around 150 mmHg or until the pulse is no longer heard. At this point blood flow in the underlying blood vessel is cut off by pressure in the cuff.

4. At around 150, slightly open the valve on the air pump (held in your left hand). This part takes practice, it’s important that you don’t let the air out too suddenly.

5. Now, pay attention to what you hear through the stethoscope as the needle on the pressure gauge falls. You will be listening for a slight “blrrp” or something that sounds like a “prrpshh”. The first time you hear this sound note the reading on the gauge. This value is the systolic blood pressure.

6. The sounds should continue and become louder in intensity. Note the reading when you hear the sound for the last time. This is the diastolic blood pressure.


Function of Vasodilation

When the smooth muscle cells in blood vessels relax during vasodilation, blood flow increases. This in turn provides more oxygen to the tissues of the body, along with other nutrients like glucose and lipids. It is used to maintain homeostasis in the body when there is a nutrient shortage in the cells or inadequate blood flow. It can also happen in response to hormones or the nervous system. For example, the parasympathetic nervous system is active during periods of rest in the body, when an organism is not experiencing a “fight or flight” response, and it allows the blood pressure and heart rate to decrease during this time. Vasodilation decreases blood pressure and heart rate because of decreased vascular resistance in the blood vessels as they expand.


Plasma is the tissue fluid of blood , It represents 54 % of the blood volume , It contains 90 % water , 1 % inorganic salts such as Ca ++ , Na + , Cl − and ( HCO3 ) − , 7% proteins as albumin , globulin and fibrinogen , 2 % other components as the absorbed food ( sugars and amino acids ) , hormones , enzymes , antibodies and wastes ( urea ) .

RBCs – Red blood cells ( Erythrocytes )

They are the most abundant blood cells , they are nearly about 4 : 5 million cell/mm³ in males , 4 : 4.5 million cell/mm³ in females , Their shape is round corpuscles and biconcave , They produced in the bone marrow of backbone .

Each cell is destroyed after 120 days , They circulate about 172,000 circulations , They are destroyed in the liver , spleen and bone marrow , They are e nucleated cells contain haemoglobin ( protein + iron ) which gives the blood its red colour .

Functions

  1. Transporting oxygen from the two lungs to all the body parts , where in the two lungs , the haemoglobin combines with oxygen to form a pale red oxyhaemoglobin ,The oxyhaemoglobin carries the oxygen to the different parts of body , where it leaves the oxygen and changes into haemoglobin .
  2. Transporting CO2 from all the body parts to the two lungs , where the haemoglobin combines with CO2 inside the body cells to form a dark red carbo-aminohaemoglobin , Carbo-aminohaemoglobin carries CO2 to the two lungs , where it leaves CO2 and changes into haemoglobin .

WBCs – White blood cells ( Leucocytes )

The number of white blood cells is 7000 cell/mm³ , this number increases during diseases , Their s hape is colourless and nucleated with many shapes , They are formed in the bone marrow , spleen and lymphatic system , some of their kinds live for 13 – 20 days .

Functions : They are produced in many types , each type with a specific function , but the main function is the protection of body against the infectious diseases thro ugh the following :

They circulate continuously in the blood vessels , attack the foreign particles , destroy and engulf them , Some of them produce antibodies .

Blood platelets

The number of blood platelets is 250 , 000 platelet /mm³ , Their s hape is non-cellular and very small in size , Their size is one fourth of the RBCs , They are produced from the bone marrow , They live for about 10 days , They play a role in blood clot after the injury .

Blood clot

Blood clot occurs when a blood vessel is cut , The i mportance of clotting : Blood forms a clot to prevent the bleeding before it leads to shock followed by death .

Factors of coagulation ( clotting ) of blood :

  1. Exposure of blood to air .
  2. Friction of blood with rough surfaces as destroyed cells & tissues .
Mechanism of blood clotting

In case of the presence of blood clotting factors , the steps are shown as the following :

The blood platelets together with the destroyed cells from a protein calle d thromboplastin .

Platelets + Destroyed cellsThromboplastin in presence of ( clotting factors in blood )

In the presence o f calcium ions ( Ca ++ ) and blood clotting factors in the plasma , thromboplastin activates the conversion of prothrombin into thrombin .

ProthrombinThrombin ( Active enzyme ) , in the presence of Thromboplastin , Ca ++ , clotting factors

Where Prothrombin is a protein that is secreted in the liver with the help of vitamin K and is passed directly into the blood .

Thrombin catalyzes the conversion of fibrinogen ( soluble protein in plasma ) into fibrin ( insoluble protein )

Fibrinogen ( Soluble protein )Fibrin ( Insoluble protein ) in the presence of Thrombin

Fibrin precipitates as a network of microscopic interlacing fibers where the blood cells are aggregated , forming a clot which blocks the cut in the damaged blood vessels .

Reasons of the non-clotting of blood inside the blood vessels
  1. Blood runs in a normal fashion inside the blood vessels without slowing down .
  2. Platelets a lso slide easily and smoothly inside the blood vessels in order not to be broken .
  3. The presence of heparin ( it is secreted by the liver ) which prevents the conversion of prothrombin into active thrombin .
Functions of blood

Transportation : It transports the digested food substances , waste nitrogenous compounds , hormones and some enzymes ( active or inactive ) through the plasma , I t transports O2 and CO2 through RBCs .

Controlling : It controls the processes of metabolism , It keeps the body temperature at 37° C , It regulates the internal environment ( homeostasis ) such as osmotic potential , amount of water and pH in the tissues .

Protection : It protects the body against the microbes and pathogenic organisms through the immunity involving the lymphatic system ( WBCs ) , It protects the blood itself against the bleeding by the formation of blood clot .

Blood Pressure

The blood is a viscous liquid which circulates within the arteries and veins smoothly by the process of heartbeats , but to pass within the microscopic blood capillaries , it needs pressure .

The maximum blood pressure is measured as the ventricles contract and the largest blood pressure is measured in the arteries nearer to the heart .

The minimum blood pressure is measured as the ventricles relax and the blood pressure in the venules i s very low ( about 10 mm Hg ) , This pressure is not sufficient to move the blood back to the heart , So , the returning of blood to the heart depends on :

  • The skeletal muscles near the veins : when these muscles contract , they put a pressure on the collapsible walls of veins and the blood contained in these vessels .
  • Valves of veins : that prevent the backward flow of blood .
Measurement of blood pressure

The blood pressure is measured by means of mercuric instruments sphygmomanometers , There readings consist of two numbers :

  • Maximum : measured during the ventricular contraction which represents the maximum blood pressure .
  • Minimum : measured during the ventricular relaxation which represents the minimum blood pressure .

Example : 120/80 mm Hg is the normal value of blood pressure in youth , so , the number of 120 mm Hg represents the ventricular contraction ( cystolic ) and 80 mm Hg represents the ventricular relaxation ( diastolic ) .

Sphygmomanometer

Structure : a mercuric tube and a scale board .

Idea of working : blood pressure can be measured according to the elevation of mercury level inside the tube and it is represented by a number on the scale board .

Method of measurement

The values of blood pressure are determined by listening to the heartbeats , and also between one beat and another , as the following :

on hearing the sound of heartbeat , the doctor can determine the maximum value of blood pressure , referring to the ventricles contraction ( cystolic ) .

When the sound disappears , the doctor can determine the minimum value of blood pressure , referring to the ventricles relaxation ( diastolic ) .

The blood pressure increases gradually by aging and it must be under medical control to avoid its harmful effects , There are some digital instruments to measure the blood pressure , but they are not accurate as the mercuric instruments .

The blood pressure in creases in arteries gradually by aging , leading to the increase of resistance against the passage of blood through them .


Digital blood pressure monitors

Digital blood pressure monitors are often used on the wrist, but they can also be placed on the finger or upper arm and are activated simply by pressing a button. They read the blood pressure automatically based on variations in the volume of blood in the arteries. When taking blood pressure measurements on the wrist, it's important to keep the hand level with the heart. Otherwise it can affect the readings.

Digital meters can sometimes be inaccurate and produce unreliable readings anyway – especially in people with certain heart rhythm problems or arteries that have hardened due to arteriosclerosis.


Related Testing

Myocardial perfusion testing is a noninvasive diagnostic evaluation performed on patients with suspected coronary artery disease. Pharmacological stimuli, most commonly adenosine, are used to assess myocardial blood flow and coronary flow reserve. Adenosine is a powerful vasodilator used in these tests to produce maximal hyperemia during imaging.[8]

Acute vasodilator testing can help to identify patients with pulmonary artery hypertension (PAH) who may respond to calcium channel blocker therapy. The testing procedure is performed during a right-heart catheterization. Vasodilatory medications are administered to assess the ability of the pulmonary arteries to relax before and after administration. Commonly used vasodilator drugs for the procedure include nitric oxide, epoprostenol, and adenosine.[9]


Unexpected discovery opens a new way to regulate blood pressure

An isolated cerebral arteriole from a mouse model, marked by a live-cell dye. Credit: Osama Harraz, Ph.D., University of Vermont Larner College of Medicine

High blood pressure, or hypertension, is the leading modifiable risk factor for cardiovascular diseases and premature death worldwide. And key to treating patients with conditions ranging from chest pain to stroke is understanding the intricacies of how the cells around arteries and other blood vessels work to control blood pressure. While the importance of metals like potassium and calcium in this process are known, a new discovery about a critical and underappreciated role of another metal—zinc—offers a potential new pathway for therapies to treat hypertension.

The study results were published recently in Nature Communications.

All the body's functions depend on arteries channeling oxygen-rich blood—energy—to where it's needed, and smooth muscle cells within these vessels direct how fast or slow the blood gets to each destination. As smooth muscles contract, they narrow the artery and increase the blood pressure, and as the muscle relaxes, the artery expands and blood pressure falls. If the blood pressure is too low the blood flow will not be enough to sustain a person's body with oxygen and nutrients. If the blood pressure is too high, the blood vessels risk being damaged or even ruptured.

"Fundamental discoveries going back more than 60 years have established that the levels of the calcium and potassium in the muscle surrounding blood vessels control how they expand and contract," say lead author Ashenafi Betrie, Ph.D., and senior authors Scott Ayton, Ph.D., and Christine Wright, Ph.D., of the Florey Institute of Neuroscience and Mental Health and The University of Melbourne in Australia.

Specifically, the researchers explain, potassium regulates calcium in the muscle, and calcium is known to be responsible for causing the narrowing of the arteries and veins that elevate blood pressure and restrict blood flow. Other cells that surround the blood vessel, including endothelial cells and sensory nerves, also regulate the calcium and potassium within the muscle of the artery, and are themselves regulated by the levels of these metals contained within them.

"Our discovery that zinc is also important was serendipitous because we'd been researching the brain, not blood pressure," says Betrie. "We were investigating the impact of zinc-based drugs on brain function in Alzheimer's disease when we noticed a pronounced and unexpected decrease in blood pressure in mouse models treated with the drugs."

In collaboration with researchers at the University of Vermont's Larner College of Medicine in the United States and TEDA International Cardiovascular Hospital in China, the investigators learned that coordinated action by zinc within sensory nerves, endothelial cells and the muscle of arteries triggers lower calcium levels in the muscle of the blood vessel. This makes the vessel relax, decreasing blood pressure and increasing blood flow. The scientists found that blood vessels in the brain and the heart were more sensitive to zinc than blood vessels in other areas of the body—an observation that warrants further research.

"Essentially, zinc has the opposite effect to calcium on blood flow and pressure," says Ayton. "Zinc is an important metal ion in biology and, given that calcium and potassium are famous for controlling blood flow and pressure, it's surprising that the role of zinc hasn't previously been appreciated."

Another surprising fact is that genes that control zinc levels within cells are known to be associated with cardiovascular diseases including hypertension, and hypertension is also a known side effect of zinc deficiency. This new research provides explanations for these previously known associations.

"While there are a range of existing drugs that are available to lower blood pressure, many people develop resistance to them," says Wright, who added that a number of cardiovascular diseases, including pulmonary hypertension, are poorly treated by currently available therapies. "New zinc-based blood pressure drugs would be a huge outcome for an accidental discovery, reminding us that in research, it isn't just about looking for something specific, but also about just looking."


One Type Of Antioxidant May Not Be As Safe As Once Thought

Certain preparations taken to enhance athletic performance or stave off disease contain an anti-oxidant that could cause harm. According to new research at the University of Virginia Health System, N-acetylcysteine (NAC), an anti-oxidant commonly used in nutritional and body-building supplements, can form a red blood cell-derived molecule that makes blood vessels think they are not getting enough oxygen.

This leads to pulmonary arterial hypertension (PAH), a serious condition characterized by high blood pressure in the arteries that carry blood to the lungs.

"NAC fools the body into thinking that it has an oxygen shortage," said Dr. Ben Gaston, UVa Children's Hospital pediatrician and researcher who led the study. "We found that an NAC product formed by red blood cells, know as a nitrosothiol, bypasses the normal regulation of oxygen sensing. It tells the arteries in the lung to 'remodel' they become narrow, increasing the blood pressure in the lungs and causing the right side of the heart to swell."

Gaston notes that this is an entirely new understanding of the way oxygen is sensed by the body. The body responds to nitrosothiols, which are made when a decreased amount of oxygen is being carried by red blood cells the response is not to the amount of oxygen dissolved in blood. He says that this pathway was designed much more elegantly than anyone had previously imagined. "We were really surprised," he said.

The research team administered both NAC and nitrosothiols to mice for three weeks. The NAC was converted by red blood cells into the nitrosothiol, S-nitroso-N-acetylcysteine (SNOAC). The normal mice that received NAC and SNOAC developed PAH. Mice missing an enzyme known as endothelial nitric oxide synthase did not convert NAC to SNOAC, and were protected from the adverse effects of NAC, but not SNOAC. This suggests that NAC must be converted to SNOAC to cause PAH.

Could regular use of NAC produce the same effects in humans? The next step is to determine a threshold past which antioxidant use becomes detrimental to heart or lung function, according to Dr. Lisa Palmer, co-researcher of the study.

"The more we understand about complexities in humans, the more we need to be aware of chemical reactions in the body," said Palmer.

According to Gaston and Palmer, NAC is being tested in clinical trials for patients with cystic fibrosis as well as other conditions and clinical trials with nitrosothiols are being planned. These results, Palmer says, should motivate researchers to check their patients for PAH.

The results also open up a range of possibilities in treating PAH. Palmer added that the signaling process could be restorative and healing if they figured out how to keep NAC from fooling the body.

"From here we could devise new ways for sensing hypoxia or we could in theory modify signaling to treat PAH," Palmer said.

The results appear in the September issue of the Journal of Clinical Investigation.


Pulmonary Artery Disease

Pulmonary artery disease is a subcategory of pulmonary vascular disease (PVD). PVD affects the veins and arteries that connect the lungs and heart. The primary symptom of PVD is shortness of breath due to an inefficient oxygen supply.

When the pulmonary circulation must constantly deal with higher-than-normal pressures a diagnosis of pulmonary hypertension is likely. This diagnosis is given when average (mean) pulmonary arterial pressures are 25 mm Hg or higher.

There are three main causes of pulmonary hypertension:

  • Pulmonary arterial hypertension
  • Pulmonary venous hypertension
  • Pulmonary embolism

Embolisms are blood clots, air bubbles, pieces of arterial plaque, or fat droplets that cause blockages in the circulatory system. Once these become trapped in a smaller blood vessel, any tissue after that point can become oxygen-starved and die off. When this happens in the lungs and no immediate treatment is given, the results can be catastrophic.

Pulmonary venous hypertension is the result of congestive heart failure or problems with the mitral valve that lies between the left atrium and left ventricle. In the latter case, blood flows back from the ventricle into the atrium – a mechanism known as regurgitation. This stops the pulmonary veins from emptying blood into the heart and so increases pulmonary vein pressure.

Pulmonary arterial hypertension (PAH) is caused by medications, toxins, genetic mutations, connective tissue disease, infection, liver disease, blood disorders, damaged lung blood vessels, and various types of heart disease.

Pulmonary hypertension can take years to develop. Symptoms progressively get worse and include:

  • Shortness of breath
  • A bluish tint to lips and skin
  • Coughing up blood
  • Fatigue and dizziness
  • Chest pain
  • Swollen ankles, legs, and abdomen
  • Rapid heart rate or palpitations

Pulmonary hypertension risk factors are:

  • Age
  • Family history of PAH
  • Obesity
  • Blood clotting problems
  • Genetic disorders
  • Medication
  • Smoking
  • Asbestos exposure
  • Living at high altitudes

When pulmonary artery pressure is high, the effects spread to the heart. Cor pulmonale describes a large right ventricle this part of the heart must work very hard to force blood through stiff and damaged pulmonary arteries. Reduced blood flow in the lungs also means that blood can develop small clots. These can block smaller vessels of either lung – a pulmonary embolism.

The heart is continuously responding to chemical and pressure messages via the autonomic nervous system. Pulmonary artery disease triggers compensation mechanisms such as a rapid heart rate. This heart rate can become irregular – arrhythmia – over time this leads to symptoms such as dizziness and fainting.

Higher pressure in the blood vessels of the lungs also damages the delicate capillaries and alveoli. Alveolar diffusion becomes compromised and oxygen supply to the heart is much less efficient. Damage to the lung capillaries means that someone with chronic pulmonary hypertension may often cough up blood.