# data[].attributes.headline
Why does cholesterol effect the bloodstream 10.1

# data[].attributes.subject
Why does cholesterol effect the bloodstream 10.1

# data[].attributes.body
-Caden

# data[].attributes.body
pump blood into a hemocoel with the blood diffusing back to the circulatory system between cells. Blood is pumped by a heart into the body cavities, where tissues are surrounded by the blood.

# data[].attributes.body
Closed circulatory systems have the blood closed at all times within vessels of different size and wall thickness. In this type of system, blood is pumped by a heart through vessels, and does not normally fill body cavities.

# data[].attributes.body
They don't have any other organelles. During the last part of red blood synthesis,

# data[].attributes.body
A closed circulatory system is much more efficient than an open circulatory system. It allows animals to grow bigger because they are able to maintain pressure in the blood vessels as opposed to open space. It also allows for an increased metabolic rate because more oxygen is available.

# data[].attributes.body
Disruption to regular blood flow can cause tissue death. Depending on which blood vessel is blocked, it can lead to death.

# data[].attributes.body
Too fast heartrate is known as tachycardia. Tachycardia (usually considered over 100 bpm in an adult) can increase risks of heart attack or stroke. When the heart pumps too fast, it is less efficient and less blood is pumped per beat.

# data[].attributes.body
If the blood clot blocks an artery, it can cause an infarction and cause local death of the tissue. There is also danger of the blood clot migrating to a vital organ (e.g. heart or lung). Migrating blood clots in veins can also cause valve damage.

# data[].attributes.body
What are the advantages of a closed circulatory system over an open circulatory system?

# data[].attributes.body
What is a closed circulatory system?

# data[].attributes.body
What is a closed circulatory system?

# data[].attributes.body
What is an open circulatory system?

# data[].attributes.body
It transport nutrients, hormones, and proteins to the parts of the body that need it.

# data[].attributes.body
This website lays it out very nice and easy to read.

# data[].attributes.attachment_link.readable_text
The heartbeat plays a key role in blood circulation. The cyclical repetition of the various changes that are taking place in heart from beat to beat is called as cardiac cycle. the cardiac cycle has two stages, they are

⦿ Contraction stage or systole

⦿ Relaxation stage or diastole.

Systole is the contraction phase of the cardiac cycle. The systole contains of two events called Atrial Systole and Ventricular Systole. The BP of 120 is considered normal in case of systolic pressure.

Diastole is the relaxation phase of the cardiac cycle. The Diastole consists of two events called Atrial Diastole and Ventricular Diastole. The BP of 80 is considered normal in case of diastolic pressure.

Systole is the contraction phase of the cardiac cycle of the heart.

Diastole is the relaxation phase of the cardiac cycle of the heart.

In systole stage, when the heart contracts, it pumps blood from the heart Chambers into the aorta and a pulmonary artery.

In Diastole stage, when the heart relaxes, it allows the heart chambers to be filled with blood from venacava and pulmonary veins.

BLOOD PRESSURE

The blood pressure of the systole stage is high.

The blood pressure of the diastolic stage is low.

AVERAGE PRESSURE

The systolic pressure for a normal person is 120.

The diastolic pressure for a normal person is 80.

FLUCTUATIONS

The systolic pressure undergoes considerable fluctuations at different conditions like the extent of work done by heart, the force at which the heart is working, etc.

The diastolic pressure undergoes much less fluctuation in health and remains within a limited range. The increase in diastolic pressure indicates that the heart is approaching towards failure.

The time duration required to complete one cardiac cycle is approximately 0.8 seconds and the heart rate of an average person is 75 beats per minute. Alterations in the cardiac output results in the changes in blood pressure which causes The conditions like hypertension, etc

# data[].attributes.attachment_link.description
The heartbeat plays a key role in blood circulation. The cyclical repetition of the various changes that are taking place in heart from beat to beat is called as cardiac cycle. the cardiac cycle has two stages, they are ⦿ Contraction stage or systole ⦿ Relaxation stage or diastole.

# data[].attributes.body
What can happen if there are disruption to our regular blood flow? Can it lead to serious damage in the body like death?

# data[].attributes.body
How many chambers in the human heart?

# data[].attributes.body
It depends how the heart is configured.  In general, if the heart has fewer chambers, it is less efficient.  For example, a 3-chambered heart (such as what is found in amphibians) mixes oxygenated and deoxygenated blood before pumping it into the body.  This is much less efficient than a 4-chambered heart.
For a human, a missing chamber means that a person will need corrective surgery as an infant or may die.

# data[].attributes.body
what is the difference between systole and diastole?

# data[].attributes.body
What happens when a blood clot occurs in an undamaged blood vessel ?

# data[].attributes.body
If the SA node does not send enough impulses the heart may beat irregularly or have long pauses between beats. Pacemakers are added by doctors to regulate fast or slow heartbeats caused by improper SA node function. Pacemakers are implanted just under the skin as shown in the picture.

# data[].attributes.body
What happens if your heart is missing one of its chambers

# data[].attributes.body
So if the SA (sinoatrial) node controls when electrical impulses are sent out causing a heartbeat, what happens when it doesn't send out enough impulses? Can pacemakers be added externally by doctors?

# data[].attributes.body
So red blood cells don't replicate? Also if they don't have a nucleus do they have any other organelles?

# data[].attributes.body
why don't mature red blood cells contain nuclei?

# data[].attributes.body
What would happen if the heartbeat goes way beyond 70 times a minute? For example, 60 or 80 times a minute. And how can it affect our body if the heart doesn't pump within the average?

# data[].attributes.body
SA Node - Mass of auto-rhythmic cells located in the right trail wall near the entrance of the superior vena cava (SA = senatorial); generates impulses about 75 times per min.

# data[].attributes.body
They don't! They don't have DNA or RNA and can't make any proteins. They are continually replenished because they are manufactured by the bone marrow that codes for the protein hemoglobin.

# data[].attributes.body
The lifespan of white blood cells is variable depending on the type of cell and whether or not it has engulfed bacteria/cells infected with viruses. Here's a link with more info:

# data[].attributes.attachment_link.readable_text
Three Classes Of Blood Cells

Human blood actually contains three different classes of cells: red blood cells for carrying oxygen, five types of white blood cells for fighting infection and platelet cells for wound clotting. As such, each type of cell has its own lifespan, from a few hours to several decades.

About the Author

A Chicago-based copywriter, Andy Pasquesi has extensive experience writing for automotive (BMW, MINI Cooper, Harley-Davidson), financial services (Ivy Funds, William Blair, T. Rowe Price, CME Group), healthcare (Abbott) and consumer goods (Sony, Motorola, Knoll) clients. He holds a Bachelor of Arts in English from Harvard University but does not care for the Oxford comma.

# data[].attributes.attachment_link.description
Human blood actually contains three different classes of cells: red blood cells for carrying oxygen, five types of white blood cells for fighting infection and platelet cells for wound clotting. As such, each type of cell has its own lifespan, from a few hours to several decades.

# data[].attributes.body
It is possible but you have to be very careful.

# data[].attributes.body
I couldn't find any other uses than blood clotting online, but the first section of this page is a really good description of their function

# data[].attributes.attachment_link.readable_text
Marlene Williams, M.D. currently applies her clinical and research expertise to platelet function and genotyping in acute coronary syndrome.
The purpose of platelets

"Platelets are the cells that circulate within our blood and bind together when they recognize damaged blood vessels," says Dr. Marlene Williams, assistant professor of medicine and CICU director at Johns Hopkins Bayview Medical Center. "When you get a cut, for example, the platelets bind to the site of the damaged vessel, thereby causing a blood clot. There's an evolutionary reason why they're there. It's to stop us from bleeding."

What makes platelets change their shape?

Platelets, the smallest of our blood cells, can only be seen under a microscope. They're literally shaped like small plates in their non-active form. A blood vessel will send out a signal when it becomes damaged. When platelets receive that signal, they'll respond by traveling to the area and transforming into their "active" formation. To make contact with the broken blood vessel, platelets grow long tentacles and then resemble a spider or an octopus.

What is a healthy platelet count?

A normal platelet count ranges from 150,000 to 450,000 platelets per microliter of blood. Having more than 450,000 platelets is a condition called thrombocytosis; having less than 150,000 is known as thrombocytopenia. You get your platelet number from a routine blood test called a complete blood count (CBC).

What it means to have too many platelets (thrombocytosis)

The medical term for having too many platelets is thrombocytosis, and there are two types:

Primary or essential thrombocytosis - Abnormal cells in the bone marrow cause an increase in platelets, but the reason is unknown

Secondary thrombocytosis - The same condition as primary thrombocytosis, but may be caused by an ongoing condition or disease such as anemia, cancer, inflammation, or infection

When there are symptoms, they include spontaneous blood clots in the arms and legs, which if untreated can lead to heart attack and stroke. In severe cases, the patient might have to undergo a procedure called a platelet pheresis. This lowers the platelet count by removing the blood, separating out the platelets, and returning the red blood cells back to the body.

With secondary thrombocytosis, the symptoms are usually related to the associated condition. For example, if you have an infection or anemia, you treat those conditions and the platelet count comes down.

What it means to have too few platelets (thrombocytopenia)

When you don't have enough platelets, it's called thrombocytopenia. Symptoms include easy bruising, and frequent bleeding from the gums, nose, or GI tract. Your platelet count drops when something is preventing your body from producing platelets. There are a wide range of causes, including:

Medications

An inherited condition

Certain types of cancer, such as leukemia or lymphoma

Chemotherapy treatment for cancer

Kidney infection or dysfunction

Too much alcohol

How platelets relate to cardiovascular disease

If you have too many platelets, it can increase your risk for clotting. But often your cardiovascular risk has more to do with platelet function than platelet number. For example, you could have a healthy number of platelets, but if they're sticking together too much it can increase your chance of having a heart attack or stroke.

Keeping track of your platelets

Too many platelets, too few platelets, abnormally functioning platelets, and related conditions such as blood clots, strokes, and heart attacks can be inherited. So it's a good idea to alert your doctor when there's a family connection.

"Although you may feel fine, your physician might want to keep a close eye on you and investigate whether or not you need medications to reduce the functioning of your platelets," says Dr. Williams. "The most common blood-thinning medication is aspirin, although recent studies have shown that women under 65 who are otherwise healthy do not receive the same benefit from aspirin as men do. There is no concrete answer to that yet."

More information

Health Library

Explore our health library for more information about conditions and treatments.

Locations

The Sheikh Zayed Tower brings the best of patient-centered medicine to the Heart and Vascular Institute.

# data[].attributes.attachment_link.keywords[]
women heart disease cardiovascular baltimore health

# data[].attributes.attachment_link.keywords[]
woman cardiovascular heart disease platelets thrombocytosis blood clot

# data[].attributes.attachment_link.title
What are Platelets and Why They are Important: Johns Hopkins Women's Cardiovascular Health Center

# data[].attributes.attachment_link.description
Marlene Williams, M.D. currently applies her clinical and research expertise to platelet function and genotyping in acute coronary syndrome. "Platelets are the cells that circulate within our blood and bind together when they recognize damaged blood vessels," says Dr. Marlene Williams, assistant professor of medicine and CICU director at Johns Hopkins Bayview Medical Center.

# data[].attributes.body
red blood cells only live around 120 days because they don't have a nuclei. White blood cells have a nuclei, would this make them live longer and if so how much longer?

# data[].attributes.body
The colour we see veins through our skin can also be affected by the colour of your skin, for instance in people with warmer toned colouring the vessels will appear green, if someone has cooler toned skin vessels may appear blue or purple

# data[].attributes.body
How do red blood cells store genetic material if they have no nucleus?

# data[].attributes.body
Is there anything else platelets do, beside helping in blood clotting?

# data[].attributes.attachment_link.readable_text
Blood is always red, actually. Veins look blue because light has to penetrate the skin to illuminate them, blue and red light (being of different wavelengths) penetrate with different degrees of success. What makes it back to your eye is the blue light.

Meanwhile, here's what happens to the blood in your body:

The heart pumps blood to your lungs to pick up oxygen. The oxygen-rich blood is then pumped out to your body through your arteries. It's bright red at this point.

From your arteries, the blood flows through tiny blood vessels called capillaries, where it gives up its oxygen to the body's tissues. Your lips have a lot of these capillaries, which is why they're red.

Your blood, now exhausted of its oxygen, is dark red as it now returns to your heart through your veins.

This article has been corrected from the original version.

Follow Life's Little Mysteries on Twitter @llmysteries. We're also on Facebook & Google+.

# data[].attributes.attachment_link.description
Blood is always red, actually. Veins look blue because light has to penetrate the skin to illuminate them, blue and red light (being of different wavelengths) penetrate with different degrees of success. What makes it back to your eye is the blue light.

# data[].attributes.body
While I don't know the exact reason, I would suspect it has to do with 2 things: 1) The temperature of blood in the body is at 37 degrees, which is more soluble than room temperature. 2) Blood is constantly being circulated. If the blood pools in an area for too long, it will start to clot and separate. Also, the separated blood that you see in diagrams is put through a centrifuge at extremely high gravity (100s of times that of earth), which is what separates it so well.

# data[].attributes.body
Red blood cells become damaged over time and may release iron into the blood stream if they are not broken down correctly in the spleen or liver. This can cause toxic levels of iron to accumulate in the blood and can cause kidney damage.

# data[].attributes.body
Why is it not possible to use animal blood for transfusion?

# data[].attributes.body
It is important to have two different types of blood cells because they serve different functions. Red blood cells ensure the transport of oxygen and carbon dioxide through the blood stream. White blood cells fight infection keeping the blood 'clean', playing a role in developing immunity.

# data[].attributes.body
What keeps our blood from separating within our body?

# data[].attributes.body
Plasma mainly maintains the blood volume as it is 90-92% water, but it also aids in pH balance, immunity and clotting.

# data[].attributes.body
Why is Plasma so important

# data[].attributes.body
Why is it important to have 2 different types of blood cells (white blood cells and red blood cells)?

# data[].attributes.body
It is said that the red blood cells only live inside our body within 120 days, what would happen if some of them remained for more than that? Will it cause a major disease or infections?

# data[].attributes.body
What will happen to the blood vessels if the person is dead.

# data[].attributes.body
Here's a website with a very in-depth look at blood transfusions that occur with mismatched blood. Apparently, it occurs in about 1/25000 transfusions. The severity is related to how much blood was transfused. It may cause kidney failure and patients may need to be moved to ICU. The transfusion should immediately be stopped and patients should be given saline to replace lost fluids.

# data[].attributes.attachment_link.readable_text
Hemolytic Transfusion Reactions (ABO incompatibility)

I. What every physician needs to know.

Introduction

Blood group antigens on red blood cell (RBC) surfaces define their immune potential. The different blood groups A, B, AB and O are based on the surface presence of antigen A, antigen B, both antigens or absence of these antigens, respectively. Corresponding to these blood groups, IgM antibodies (anti-A, anti-B) are found in the plasma of adults lacking the corresponding antigen. Hence, blood group A, B, O, and AB have anti-B, anti-A, both, or none of the isoagglutinins (Rule of Landsteiner). Apart from these, there are 'minor' alloantibodies such as anti-D, anti-K, and anti-Jka which are present in varying proportions in the population.

Transfusion of blood components can cause a multitude of reactions, not all of which are immune-mediated and not all of which lead to hemolysis (see "Transfusion reactions"). Transfusion entails the merging of two antigenically charged pools of blood components - donors with recipients - thus pre-transfusion compatibility testing is essential to minimize interactions.

Compatibility testing pre-transfusion involves blood typing and cross-match (via the indirect antiglobulin test - see Coombs test below) to ensure the recipients' blood lacks antibodies that can react with donor antigens and lead to destruction of transfused cells. In spite of compatibility testing, a conglomeration of system and process errors may still lead to transfusion of mismatched blood leading to incompatibility reactions, generally as a clerical or procedural error.

Key definitions

Hemolytic transfusion reactions (HTRs): The occurrence of a serologic reaction (acute reaction) or alloimmunization (delayed reaction) as a result of blood component therapy which leads to a clinically relevant acute or delayed decrease in RBC survival.

Delayed serologic transfusion reactions (DSTRs): The occurrence of alloimmunization as a result of blood component therapy without any associated hemolytic anemia.

Types of hemolytic transfusion reactions

Immune mediated hemolytic transfusion reactions

These can be acute or delayed in onset:

Acute HTRs: These are due to preformed antibodies against donor RBC antigens present in the recipient's blood. ABO incompatibility reactions are the most dreaded hemolytic transfusion reactions due to their ability to cause intravascular hemolysis. Non- ABO incompatibility reactions due to minor recipient antibodies (anti-Rh, anti-Kidd or anti-Jka) tend to be milder and generally lead to extravascular hemolysis of the antibody coated RBCs. However, occasionally high titers of these antibodies may involve complement fixation and intravascular HTRs.

Delayed HTRs: These are due to an anamnestic response to donor RBC antigens which produces antibodies after a lag period of 3-10 days. This requires prior sensitization in the form of pregnancy, transplantation or transfusions.

Non-immune-mediated hemolytic transfusion reactions

These are generally related to improper storage and handling of blood leading to hemolysis in vitro prior or during transfusion:

Thermal injury: During re-warming of the blood if temperatures reach more than 42°C

Cold injury: Inappropriate storage with exposure to ice or temperatures less than 6°C

Mechanical injury: Lysis during transfusion through small-bore catheters.

Concomitant drug-induced hemolysis

Concomitant administration of hypotonic solutions (D5%W, hypotonic saline) leading to osmotic injury

Pathophysiology of ABO incompatibility HTRs

The A and B antigens are the most immunogenic; hence transfusion of an ABO incompatible unit causes the recipient antibodies to interact with the donor RBC surface antigens, triggering complement activation and resulting in the acute intravascular hemolysis of the transfused donor RBCs.

Complement activation causes various pro-inflammatory effects via release of active C3a and C5a subcomponents. These are anaphylatoxins which cause histamine and serotonin release from mast cells, increase vascular permeability causing a capillary leak syndrome and stimulate smooth muscle contraction. These translate clinically into the classical symptoms of flushing, hypotension and bronchospasm, respectively.

Experimental evidence supports a central role for cytokines in the pathophysiology of hemolytic transfusion reactions. Tumor necrosis factor (TNF) appears to be the most commonly identified mediator of intravascular coagulation and end-organ injury although other cytokines have been implicated including interleukin (IL)-8, monocyte chemoattractant protein, and IL-1 receptor antagonist.

Ultimately, the complement cascade terminates with activation of the membrane attack complex (MAC) leading to cytolysis. The released hemoglobin tetramers complex with haptoglobin and are removed by the liver, causing haptoglobin depletion. Residual free hemoglobin circulates in the plasma or gets converted to oxidized methemoglobin in the blood, imparting a reddish or brownish color, respectively.

Small, unbound hemoglobin dimers are also filtered by the glomerulus which causes hemoglobinuria. This heme pigment causes acute kidney injury directly or via tubular obstruction or vasoconstriction. In practice, this heme-induced acute tubular necrosis requires a secondary factor like dehydration, nephrotoxin use or sepsis to translate into significant renal insufficiency.

The hemoglobin is taken up by the renal tubular cells, degraded and the iron is stored as hemosiderin. When these renal tubular cells are sloughed in the urine 3-10 days later, hemosiderinuria becomes detectable.

Tissue factor is expressed on monocytes and endothelial cells and can precipitate disseminated intravascular coagulation (DIC). The exposure of RBC stroma and cytokine activation may also feed the consumptive coagulopathy. In rare cases, the above events may culminate into multi-organ failure.

II. Diagnostic Confirmation: Are you sure your patient has ABO incompatibility?

The following criteria determine occurrence of an ABO incompatibility reaction:

1) Recent or ongoing transfusion of blood products.

2) Acute onset of fever or hemodynamic instability.

3) Evidence of hemolysis on visual examination of blood samples and urine.

4) Evidence of hemolysis on laboratory investigations.

5) A positive Coombs test on recipients' blood.

A. History Part I: Pattern Recognition:

The symptoms of acute hemolytic transfusion reactions can be initially nonspecific and difficult to differentiate from other transfusion reactions. However, always rule out ABO incompatibility, especially if the reaction is severe. Serious transfusion reactions can develop within minutes of starting a transfusion; therefore, monitoring vital signs on initiation and within the first 15 minutes of a transfusion is essential.

Symptoms due to the serologic reaction and complement activation

Fevers are the most common presenting symptom and close vigilance can abort a transfusion before severe damage is done. ABO incompatibility reactions resemble any other drug reaction initially with malaise, dizziness, chills, backache and anxiety.

Vital signs may reflect systemic inflammatory response syndrome (SIRS) criteria with tachycardia and tachypnea. The anaphylatoxins cause bronchospasm with dyspnea, hypotension, flushing, chest pain, and nausea.

Symptoms of complications due to hemolysis

Since HTRs cause hemolysis of the small volume of donor cells, the main threat is not that of low hemoglobin but that of pigment-induced injury due to the intravascular hemolysis. Depending on the extent of intravascular hemolysis, one could see rapid development of hemoglobinuria and patients may complain of a darkening of urine. Dark urine may be the first indicator of intravascular hemolysis, especially in anaesthetized or unconscious patients. Oliguria is noted on subsequent monitoring as acute renal failure sets in.

Patients with severe ABO incompatibility may develop DIC and show all the symptoms of this disease, including diffuse bleeding. Fatality is rarely seen in modern medicine but would be due to a multiorgan failure following circulatory shock.

In contrast to ABO incompatibility, DHTRs cause extravascular hemolysis and are generally asymptomatic and rarely fatal. Fever and chills are common a week or two after initial blood transfusion and are associated with a decreasing hemoglobin and spherocytosis. Hyperbilirubinemia may be seen but discoloration of the urine is rare due to extravascular hemolysis. Due to the nonspecific signs and symptoms, DHTRs tend to go unrecognized.

B. History Part 2: Prevalence:

Approximately one of every 25,000 transfusions is complicated by ABO incompatibility. Blood group O and A are the most prevalent in the community, accounting for 43% and 44% of the population. Based on this, the most common mismatches are due to transfusion of type A blood to type O individuals who carry both anti-A and anti-B. The reverse scenario, i.e., transfusion of type O blood to type A blood group individuals, is acceptable since group O is antigenically silent.

Any patient receiving a transfusion, irrespective of type and cross-match, remains at risk for incompatibility reactions since most of these are due to clerical or procedural errors, i.e., wrong blood to wrong patient. However certain patients may be particularly at risk.

Specific at-risk patient populations

Emergencies where O group blood is transfused while a concurrent blood cross-match is being performed in the laboratory.

Short supply of the patient blood type.

Solid organ transplantation.

ABO mismatched platelet transfusion.

Age distribution of ABO incompatibility reactions

Newborns develop antibodies to RBC antigens A and B after 3-4 months of life and hence life threatening ABO-related transfusion reactions are not observed in this age group.

At the other extreme there is a steady decline in the titers of ABO antibodies after age 60 which decreases the severity of these reactions. However, most blood transfusions are administered to persons aged 60 years and older; therefore, most acute transfusion reactions also occur in this age group.

C. History Part 3: Competing diagnoses that can mimic ABO incompatibility

1. Any transfusion reaction, including febrile non-hemolytic transfusion reactions and allergic reactions, should be considered in the early differential. They should be differentiated from each other only when laboratory data is available and as the clinical course evolves.

2. Concurrent drugs or inherent patient conditions which may precipitate hemolysis.

3. In trauma patients receiving blood transfusions it may not be uncommon to see hemodynamic instability, acute renal failure and discolored heme-positive urine from rhabdomyolysis. Also, in patients with trauma who are being transfused blood, it may become necessary to distinguish between myoglobinuria and hemoglobinuria both of which can cause urine color changes and a heme-positive dipstick result.

D. Physical Examination Findings.

HTRs may not reveal any specific examination findings. Patients may have fever, rigors, and hemodynamic instability. Jaundice may be apparent. Pulmonary auscultation may reveal wheezing.

E. What diagnostic tests should be performed?

1. What laboratory studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

Transfusion reactions are acute, varied in etiology, and require urgent treatment. This establishes a diagnostic urgency for the practicing physician and requires collaboration with the blood bank and pathologists. However, it needs to be stressed that treatment should be initiated at the earliest without awaiting the final diagnosis.

Steps to diagnosis

The following steps should be undertaken to arrive at the diagnosis:

1) Examining the blood product bag

Since most of the HTRs are due to clerical/process errors, verifying the blood bag identity with the patient identifiers reveals the incompatibility in most cases.

2) Screening tests

Complete blood count with peripheral smear

Comprehensive metabolic panel

Urinalysis

Hemolysis panel (haptoglobin and LDH)

3) Confirmatory tests

The direct Coombs test is the diagnostic test for ABO incompatibility reactions.

4) Evaluate competing diagnosis

Though the temporal relationship of the blood transfusion is a good surrogate for an etiologic cause, concurrent drugs and inherent patient conditions may also induce hemolysis in a few patients. A comprehensive evaluation will ensure that alternative etiologies are not missed. (See destructive anemias)

Overview of laboratory tests

1) Complete blood count

Since the volume of the lysed donor PRBCs is small, HTRs do not cause a significant drop in the hemoglobin. Occasionally, a non-significant increase in the hemoglobin post-transfusion can hint towards a HTR with the right clinical picture. Platelet counts and coagulation abnormalities become evident if DIC sets in.

A peripheral blood smear can detect schistocytes and shift cells which are large polychromatic RBCs, suggestive of early release of reticulocytes into the circulation due to erythropoietin stimulation.

2) Comprehensive metabolic panel

An elevation in the unconjugated bilirubin may indicate hemolysis. Hyperkalemia may develop from cell lysis. A basic metabolic panel also provides a baseline creatinine to help monitor for the onset of acute renal failure.

3) Urinalysis

Urinalysis may show hemoglobinuria. Normally hemoglobin does not undergo glomerular filtration due to its large molecular size; however, during high plasma concentrations due to ongoing hemolysis it can be transiently detected in the urine. Depending on the concentration and its state of oxidation, the urine color changes from pink-red to a dark brown, while severe cases of intravascular hemolysis can classically show very dark urine termed "blackwater".

Degraded hemoglobin gets deposited into the tubular cells as hemosiderin. After 3-7 days, as the tubular cells slough off, hemosiderinuria can be detected by iron staining of the urine.

4) Other tests indicating presence of acute intravascular hemolysis

Elevated LDH and decreased haptoglobin can correlate with the degree of hemolysis. Note that haptoglobin is also an acute phase reactant and may be relatively elevated by a concomitant inflammatory condition.

Hemoglobinemia imparts a pinkish color to the plasma. This requires high levels of free hemoglobin and may be masked by concurrent bilirubin. On automated cell counters it causes a rise in mean corpuscular hemoglobin concentration (MCHC). RBC lysis during venipuncture can also show hemoglobinemia in the blood sample.

The above tests for hemolysis may be less reliable in patients with concomitant liver disease who also have low haptoglobin levels, high bilirubin and high LDH. However serial measurements of these may indicate an active hemolysis.

5) Definitive diagnostic test for incompatibility

Detection of isoagglutinins attached to the RBC surface by the direct Coombs test is the best diagnostic test. However, it can be time-consuming in the setting of an obvious emergent clinical situation and treatment should be initiated at the earliest.

A repeat cross-match with the donor blood should be performed with the indirect Coombs test which detects if potential antibodies against donor RBCs were present in the patient's serum prior to transfusion.

Coombs test (Anti-globulin test)

There are two types of Coombs test - direct and indirect. The direct Coombs test is the diagnostic test for ABO incompatibility reactions. The indirect Coombs test is used for the pretransfusion cross-match or "screen" to detect the presence of antibodies in the recipient prior to a transfusion.

Direct Coombs test detects if antibodies in the blood have coated the donor RBCs. When antibodies to the human globulin fractions (antiglobulin or Coombs serum) are added to the patient's blood, they will bind to the surface antibodies and complement particles and cause the donor RBCs to agglutinate. The results are quantified on a scale from 1+ to 4+ indicating a positive test. Absence of agglutination or clumping rules out an antibody-mediated hemolysis. If there has been widespread hemolysis of the donor RBCs, the direct Coombs may be negative. In this case, the precipitous decline in the antibody titres from pre-transfusion levels can help in diagnosis.

III. Default Management

A. Immediate management

If there is a likelihood of an ABO incompatibility reaction, treatment should be initiated while awaiting laboratory data.

In general, the following steps should be followed:

1) The severity of HTRs is generally related to the volume of blood transfused, hence the most important thing is to stop the transfusion and immediately alert the blood bank.

2) Generally, all blood banks have a protocol in place to further evaluate potential HTRs which should be activated and strictly adhered to. A mismatched unit on your patient suggests that there may be another patient at risk for a mismatched unit.

3) Hemodynamic stability should be the prime concern along with ensuring an adequate airway and intravenous access. Patient should be moved to a telemetry monitored unit.

4) Treatment starts with aggressive fluid replacement with normal saline to prevent renal failure. Ringers lactate should be avoided to trigger calcium-induced clotting of the blood in the tubing. Similarly, dextrose solutions can worsen hemolysis of blood in the tubing. The initial rate could be 100ml/hr to 150ml/hr with intermittent fluid boluses to maintain a brisk urine output and avert renal failure.

5) The intravenous tubing, transfusion records (if on paper), donor blood bag should be preserved and sent down to the blood bank.

6) A fresh sample of the patient's blood from the opposite arm should be sent to the blood bank and blood and urine laboratory investigations should be ordered.

7) Complications should be anticipated, monitored for and treated promptly:

Widespread hemolysis can induce circulatory shock which may require vasopressor support.

The release of large amounts of potassium and other electrolytes can cause cardiac arrhythmias and may require urgent hemodialysis.

DIC should be treated supportively. See DIC

8) If the patient develops complications of acute renal failure, DIC or multi-organ failure, transfer to a higher level of care or intensive care unit may be appropriate.

9) There are some case reports of treatment of ABO incompatibility with eculizumab, a potent C5 inhibitory antibody. This may be considered in consultation with a Hematologist.

C. Laboratory Tests to Monitor Response To, and Adjustments in, Management

Monitoring of vital signs every 4-6 hours with a daily creatinine and hemoglobin may be sufficient in hemodynamically stable patients. Hemolytic data like LDH may help chart the course of the reaction; however, these tests are not routinely needed. Patients should be maintained on telemetry until the risk of acute renal failure and electrolyte abnormalities dissipates.

D. Long-term management

Preventing hemolytic transfusions reactions

HTRs can also happen due to any systematic error along the transfusion chain, from initial request for blood to actual transfusion. Generally, the actual type and screen process is not faulty. Subsequent human and process errors can occur around the two main events - specimen collection from recipient and administration of blood.

The two most common reasons for HTRs due to incompatibility are:

To target the first shortcoming, a common practice followed by many blood banks is to perform a concurrent blood typing from the other arm for first time transfusion recipients to ensure correct identification of blood type and minimize unrealized system errors.

Once the appropriately crossmatched blood is released, labelled with intended recipient information, stringent patient identification and matching via 2 separate indicators (medical record number, birth date, etc.,) will ensure that there is no mismatch. Two practitioners and if possible, the patient, should verify the match with the information printed on the blood bag.

Early detection of hemolytic transfusion reactions

Repeated studies have found no merit in using pre-transfusion prophylactic antipyretics. In fact, they can mask early constitutional symptoms of a reaction and delay life-saving treatment. Hence, these should be avoided.

Similarly, in non-emergent settings, it is essential to ensure that the patient is afebrile prior to transfusion to avoid confusing this with fever from a transfusion reaction. Also, as mentioned before, since most reactions occur within the first 15 minutes, patients' vitals should be closely monitored during this time and patients should be informed to report any new symptoms.

Post-hemolytic transfusion reaction analysis

If a patient develops a HTR, use of a sentinel error reporting system (SERS) and ensuring a root cause analysis is performed to decipher the weakest links in the transfusion chain is essential.

In cases of DHTRs, work-up should confirm the antibody formation and provide patients with a list of detectable antibodies to prevent HTRs in the future via transfusions at other medical centers.

IV. Special situations

Hyperhemolytic transfusion syndrome

Hyperhemolysis syndrome is defined as destruction of transfused as well as autologous red blood cells, leading to a precipitous drop in hemoglobin to below pre-transfusion levels. Patients with sickle cell disease present a unique sub-population at risk for hemolytic transfusion reactions due to the following reasons:

1. They tend to have repeated exposure to blood transfusions, resulting in high titers of alloantibodies.

2. There is a discrepancy in the United States between RBC phenotypes of donors (primarily non-African American) and sickle cell recipients (primarily African American), increasing risk of alloimmunization.

This syndrome is rarely seen in patients without underlying hemoglobinopathy. Sickle cell patients are at risk of developing the hyperhemolytic transfusion syndrome which involves a post-transfusion accelerated drop in hemoglobin with a sickle crisis exacerbation due to:

1. Hemolysis of donor RBCs.

2. Hemolysis of autologous RBCs due to high titers of alloantibodies with complement activation.

3. Suppression of hematopoiesis due to the transfusion itself.

These patients can be challenging to manage since additional transfusion may be required to treat anemia but carries the risk of fueling the immune reaction. A prompt Hematology consultation is appropriate. In a few case reports further transfusions have been avoided with the use of corticosteroids and intravenous immunoglobulin (IVIG) or treatment with eculizumab.

ABO mismatched platelet transfusions

Due to limited availability of platelet products they are generally transfused across the ABO barriers. Hence, single donor platelets which tend to have 200-400 ml of plasma can rarely cause ABO-incompatibility hemolytic reactions. Awareness of this possibility is key since the management remains the same.

V. Transitions of Care

D. Arranging for Clinic Follow-up

The patient should be provided with contact information for the hospital's blood bank. In the case of minor incompatibility, once the complete antibody screens are available it is essential to inform patients about the new antibodies detected. They should be instructed to provide this list when they undergo future transfusions at a different center.

VI. Patient Safety and Quality Measures

A. Core Indicator Standards and Documentation.

Ensuring proper patient identification prior to blood transfusions by matching the blood product to the patient is listed as a Joint Commission National Patient Safety Goal for 2016.

"Updated National Patient Safety Goals". http://www.jointcommission.org.

Weinstock, C, Möhle, R, Dorn, C, Weisel, K. "Successful use of eculizumab for treatment of an acute hemolytic reaction after ABO-incompatible red blood cell transfusion". Transfusion. vol. 55. 2015. pp. 605-610.

(This article gives a case report of successful treatment with eculizumab to prevent C5 activation and extend the lifetime of transfused incompatible cells.)

Boonyasampant, M, Weitz, I C, Kay, B, Boonchalermvichian, C. "Life-threatening delayed hyperhemolytic transfusion reaction in a patient with sickle cell disease: effective treatment with eculizumab followed by rituximab". Transfusion. vol. 55. 2015. pp. 2398-2403.

Eberly, L, Osman, D, Collins, N.. "Hyperhemolysis Syndrome without Underlying Hematologic Disease". Case Reports in Hematology. 8 February 2015.

# data[].attributes.attachment_link.description
Introduction Blood group antigens on red blood cell (RBC) surfaces define their immune potential. The different blood groups A, B, AB and O are based on the surface presence of antigen A, antigen B, both antigens or absence of these antigens, respectively.

# data[].attributes.body
Here's an image I found that shows the blood clotting process (Click to enlarge)

# data[].attributes.body
A condition known as hypovolemic shock can occur. This condition can cause the heart to not be able to pump enough blood throughout the body, leading to tissue and organ damage. Your heart can be damaged or you could die.

# data[].attributes.body
Here's an image I found to describe blood clotting:

# data[].attributes.headline
Why do some veins appear blue, purple, or green underneath skin?

# data[].attributes.subject
Why do some veins appear blue, purple, or green underneath skin?

# data[].attributes.body
What will happen to our heart if a person experience massive blood loss.

# data[].attributes.body
The veins are not a high pressure system like the arteries. The greater diameter allows for more blood to travel with less resistance.

# data[].attributes.body
A blood vessel wouldn't be dislocated, but may be torn or damaged. If there is an injury that effects blood vessels, they can cause internal or external bleeding which can be fatal. Certain injuries could also completely stop blood flow towards a certain limb. Depending on the severity of the injury, you could get a simple bruise or even die.

# data[].attributes.body
What can cause blood to clot when blood vessels burst?

# data[].attributes.body
What part of intrinsic conduction system starts the heart beat?

# data[].attributes.body
The tissues around the vessels also contribute to the look of some vessels as purple or blue.

# data[].attributes.body
What would happen if a person dislocated one of their blood vessels? Will they be able to survive or are there any cures for that?

# data[].attributes.body
Is there a reason why the veins have more space inside than arteries? Like, is it for a more specific function?

# data[].attributes.body
When you pop multiple blood vessels, intense bruising can occur, as well as other major symptoms like: pain, lumps, and darkening of the skin, that do require medical attention.

# data[].attributes.body
What happens if you pop multiple blood vessels?

# data[].attributes.body
Because arteries and capillaries are under much more pressure due to the amount of blood flowing through them. Veins are not under this much pressure, therefore are able to have thinner walls.

# data[].attributes.body
Why are vein's walls thinner than capillaries and arteries walls?

# data[].attributes.body
Also because arteries pump the blood around the body they are under pressure and will squirt the blood (often quite powerfully), unlike veins where any blood will ooze out with less power. This means that a cut artery can make you lose blood very fast.

# data[].attributes.body
But they can also form when they aren't needed and cause a heart attack, stroke, or other serious medical problems.

# data[].attributes.body
It is suggested that trypsinized red blood cells can reverse agglutination... Something like that. There isn't too much info on this topic.

# data[].attributes.body
Blood clots occurs very often in veins because we rupture a lot of them partially every day and it prevents Internal bleeding

# data[].attributes.body
"google it"
-teacher

# data[].attributes.body
Had there been cases of the said condition?

# data[].attributes.body
Is agglutination reversible? If so... How? Or, why not?

# data[].attributes.headline
It would lead to tissue rejection so your white blood cells will effectively have kinda a self-destruct kind of effect destroying the foreign blood cells causing you to die(maybe)

# data[].attributes.subject
It would lead to tissue rejection so your white blood cells will effectively have kinda a self-destruct kind of effect destroying the foreign blood cells causing you to die(maybe)

# data[].attributes.body
- marvin

# data[].attributes.body
Transfusing the wrong blood type can cause agglutination of the blood.  The body's immune system basically attacks the new type of blood.  It can be very serious and can be lethal.

# data[].attributes.headline
Your heart and the valves in them help to regulate it to some effect

# data[].attributes.subject
Your heart and the valves in them help to regulate it to some effect

# data[].attributes.body
-Marvin

# data[].attributes.body
I mean blood types

# data[].attributes.headline
Yes because arteries are bigger than veins so you bleed more from it 

# data[].attributes.subject
Yes because arteries are bigger than veins so you bleed more from it 

# data[].attributes.body
- Marvin

# data[].attributes.body
O2 poor blood is essentially just blood that isn't oxygenated, whereas O2 rich blood is oxygenated blood.

# data[].attributes.body
O positive is the most common (38%)
AB negative is the least common  (1%)

# data[].attributes.body
No it's just easier to show whether it's oxygenated or deoxygenated blood - mavin

# data[].attributes.body
How do veins have to ensure blood is returned at same rate of speed as it was pumped?

# data[].attributes.body
but if the arteries are cut, it can have severe consequences right?

# data[].attributes.body
It will lead to death

# data[].attributes.headline
do you mean types of blood or blood types 

# data[].attributes.subject
do you mean types of blood or blood types 

# data[].attributes.body
The sphincter opens and closes the entrance to the capillary, by which contraction causes blood flow in a capillary.
- Tobi

# data[].attributes.body
What happens if the wrong blood type is transfused to a patient?

# data[].attributes.body
What are some things that happens when a clot occurs in blood vessels

# data[].attributes.body
One can not be more important than the other because one flows to and the flows away cause it's a closed circulatory
system- Marvin

# data[].attributes.body
Why do the capillaries have sphincters?

# data[].attributes.headline
what is the most common and least common type of blood?

# data[].attributes.subject
what is the most common and least common type of blood?

# data[].attributes.body
-rachelle

# data[].attributes.body
is there actual purple veins/arteries in the circulatory system?

# data[].attributes.body
Which is the most important out of the capillaries, the arteries, and the blood vessels

# data[].attributes.body
Veins flow towards the heart and have valves, whereas arteries flow away from the heart and don't have valves. They also differ in the amount of smooth muscle in their walls (see pic below)

# data[].attributes.body
what is the difference between o2-poor blood and o2-rich blood

# data[].attributes.body
is there a replacement in veins for the loss of smooth muscle and connective tissue?

# data[].attributes.body
What is the difference between veins and arteries?