CV+ Blood
What happens in MI-
A heart attack (myocardial infarction) is usually caused by a blood clot, which stops the blood flowing to a part of your heart muscle. You should call for an ambulance immediately if you develop severe chest pain. Treatment with a clot-busting medicine or an emergency procedure to restore the blood flow through the blocked blood vessel are usually done as soon as possible. This is to prevent or minimise any damage to your heart muscle. Other treatments help to ease the pain and to prevent complications. Reducing various risk factors can help to prevent a myocardial infarction. If you have a myocardial infarction (heart attack), a coronary artery or one of its smaller branches is suddenly blocked. The part of the heart muscle supplied by this artery loses its blood (and oxygen) supply if the vessel is blocked. This part of the heart muscle is at risk of dying unless the blockage is quickly removed. When a part of the heart muscle is damaged it is said to be infarcted. The term myocardial infarction (MI) means damaged heart muscle. If a main coronary arteries is blocked, a large part of the heart muscle is affected. If a smaller branch artery is blocked, a smaller amount of heart muscle is affected. After an MI, if part of the heart muscle has died, it is replaced by scar tissue over the next few weeks.
What happens in dysrhythmias- A cardiac dysrhythmia is an abnormal heart beat: the rhythm may be irregular in its pacing or the heart rate may be low or high. Some dysrhythmias are potentially life threatening while other dysrhythmias (such as sinus arrhythmia) and normal.
Tachycardia is a fast (over 100 beats per minute) heart rhythm. Tachycardias can originate in the atria or ventricles. * Dysrhythmias that originate in the atria are termed supraventricular dysrhythmias (supraventricular means above the ventricles). These dysrhythmias include:

* Atrial flutter * Atrial fibrillation * Paroxysmal Supraventricular tachycardia * Wolff-Parkinson-White syndrome * Ventricular dysrhythmias begin in the ventricles and include: * Ventricular fibrillation * Premature ventricular contractions * Long QT syndrome

Bradycardia is a slow (under 60 beats per minute) heart rhythm. * Bradyarrhythmias are slow heart rhythms arising from disease in the cardiac electrical conduction system. Bradyarrhythmias include: * Sinus bradycardia * Conduction Block * Sick Sinus Syndrome
A premature Beat is an extra beat, occurring earlier than normal. Despite being an extra beat, patients may indicate feeling a skipped beat.
What happens in chest trauma- The major pathophysiologies encountered in blunt chest trauma involve derangements in the flow of air, blood, or both in combination. Sepsis due to leakage of alimentary tract contents, as in esophageal perforations, also must be considered.
Blunt trauma commonly results in chest wall injuries (eg, rib fractures). The pain associated with these injuries can make breathing difficult, and this may compromise ventilation. Direct lung injuries, such as pulmonary contusions (see the image below), are frequently associated with major chest trauma and may impair ventilation by a similar mechanism. Shunting and dead space ventilation produced by these injuries can also impair oxygenation.
Space-occupying lesions (eg, pneumothorax, hemothorax, and hemopneumothorax) interfere with oxygenation and ventilation by compressing otherwise healthy lung parenchyma. A special concern is tension pneumothorax in which pressure continues to build in the affected hemithorax as air leaks from the pulmonary parenchyma into the pleural space. This can push mediastinal contents toward the opposite hemithorax. Distortion of the superior vena cava by this mediastinal shift can result in decreased blood return to the heart, circulatory compromise, and shock.
At the molecular level, animal experimentation supports a mediator-driven inflammatory process further leading to respiratory insult after chest trauma. After blunt chest trauma, several blood-borne mediators are released, including interleukin-6, tumor necrosis factor, and prostanoids. These mediators are thought to induce secondary cardiopulmonary changes.
Blunt trauma that causes significant cardiac injuries (eg, chamber rupture) or severe great vessel injuries (eg, thoracic aortic disruption) frequently results in death before adequate treatment can be instituted. This is due to immediate and devastating exsanguination or loss of cardiac pump function. This causes hypovolemic or cardiogenic shock and death.
Sternal fractures are rarely of any consequence, except when they result in blunt cardiac injuries.

What happens in cardiopulmanary arrest - * Sudden cardiac arrest is a situation that occurs when the heart suddenly stops beating effectively and blood is not circulated by the heart; about 95% of individuals that have sudden cardiac arrest die from this condition. * Sudden cardiac arrest is usually due to an arrhythmia (irregular heartbeat) that causes the heart to stop pumping blood to the body. * Undiagnosed coronary artery disease is a major risk factor for sudden cardiac arrest * People at risk for sudden cardiac arrest include individuals with coronary artery disease, severe physical stress, individuals with electrical or structural changes in the heart, and those with inherited cardiac disorders. * The first sign of sudden cardiac arrest may be loss of consciousness (fainting) and/or no heartbeat or pulse; some individuals may have a racing heartbeat, dizziness, chest pain and shortness of breath, nauseaor vomiting before a sudden cardiac arrest occurs - many individuals have no signs whatsoever and simply collapse. * Sudden cardiac arrest is usually diagnosed after it occurs: physicians may utilize tests such as EKG's, MUGA, cardiac catheterization,electrophysiology tests and blood tests on those patients that survive an arrest to determine underlying causes. * Treatment of a sudden cardiac arrest requires a defibrillator to shockthe heart to restore a normal rhythm to the heart; this defibrillationmust be done within a few minutes of the sudden cardiac arrest to be effective. * Preventing sudden cardiac arrests centers on reducing the known causes that contribute to cardiac arrest such as lifestyle changes to prevent coronary artery disease, healthy diets, reducing stress, and getting regular exercise; for individuals with heart problems, taking the appropriate medications and adjusting their lifestyle may reduce risk – some individuals that have survived a sudden cardiac arrest and a few others that have electrophysiological problems may benefit from an implanted cardiac defibrillator (ICD) that detects arrhythmias automatically and then shock the patient's heart back into a normal rhythm.

Heart Sounds
Differentiating Sounds-
Begin auscultation at the apex of the heart in the fifth intercostal space to the left of the sternum. Listen with the bell of the stethoscope. Then, proceed to the tricuspid area and up the left sternal border to the second intercostal space of the pulmonic on the left and aortic on the right.
The first and second heart sounds, S1 and S2, differentiate the physiologic process of systole and diastole. Appreciate the sound of S1 in all areas before attempting to discern S2. Now, listen with the diaphragm of the stethoscope in reverse order and differentiate S1 and S2. The diaphragm is used to hear higher pitched sounds.
With the primarily passive blood flow through the tricuspid and mitral valves and the resulting increase in intraventricular pressure, which overcomes that within the atria, the valves close rapidly. This is the first heart sound of S1 and is best heard at the fifth intercostal space to the left of the sternum at the apex. As these valves close, the increased pressure causes the aortic and pulmonary valves to open and blood to flow through the large vessels into the circulation. The brief period of higher pressure in these vessels at the end of systole overcomes that in the ventricles and causes these valves to snap shut. This produces the second heart sound of S2 and diastole, which is heard best at the base of the heart, the area between the apex and the sternum.
While valve closure occurs somewhat simultaneously, it is important to remember the sounds change as a result of the pressure exerted in the heart chambers and the ultimate effects, both normal and abnormal, it has on the valves.
To put this in perspective, during normal function, the left side of the heart is a higher pressure system than the right. Because of this, the mitral valve closes slightly before the tricuspid in S1. And, the aortic valve closes slightly before the pulmonary valve in S2. Pathology in any of the valves can change the timing of closure causing a split sound, such as with atrial septal defect or a murmur most often associated with stenosis or damage.
While diastole is usually longer than systole, during periods of tachycardia it may be difficult to discern S1from S2 and ventricular filling times will decrease. The sound heard while listening to the heart and palpating a radial pulse will be that of S1. When the pulse disappears, that sound will be S2.2 Listening to the sound ofS1 in various areas of the heart and then repeating this same auscultation technique for S2 will help with recognizing normal before assessing for abnormal.
The third heart sound of S3 occurs slightly after S2, early in diastole and is best heard with the bell of the stethoscope in the mitral and tricuspid areas. While usually normal in those under age 35, it is often associated with heart failure, mitral regurgitation or pericarditis.3 This low frequency sound results from increased atrial pressure leading to increased flow rates.4 The "lub du bub" sound is often referenced to the same cadence as the word "Kentucky."
The fourth heart sound of S4 is heard slightly before S1 and is a presystolic sound in late diastole. Heard best over the apex of the heart, it is a low-pitched sound and associated with stiff ventricles from hypertrophy, ischemic or dilated cardiomyopathy. The cadence of the sound is similar to the inflections of the word "Tennessee."

S1
The first heart sound, or S1, forms the "lub" of "lub-dub" and is composed of components M1 and T1. Normally M1 precedes T1 slightly. It is caused by the sudden block of reverse blood flow due to closure of the atrioventricular valves, i.e. tricuspid and mitral (bicuspid), at the beginning of ventricular contraction, or systole. When the ventricles begin to contract, so do the papillary muscles in each ventricle. The papillary muscles are attached to the tricuspid and mitral valves via chordae tendineae, which bring the cusps or leaflets of the valve closed; the chordae tendineae also prevent the valves from blowing into the atria as ventricular pressure rises due to contraction. The closing of the inlet valves prevents regurgitation of blood from the ventricles back into the atria. The S1 sound results from reverberation within the blood associated with the sudden block of flow reversal by the valves.[1] If M1 occurs slightly after T1, then the patient likely has a dysfunction of conduction of the left side of the heart such as a left bundle branch blockage.
S2
The second heart sound, or S2, forms the "dub" of "lub-dub" and is composed of components A2 and P2. Normally A2 precedes P2especially during inspiration where a split of S2 can be heard. It is caused by the sudden block of reversing blood flow due to closure of the semilunar valves (the aortic valve and pulmonary valve) at the end of ventricular systole and the beginning of ventriculardiastole. As the left ventricle empties, its pressure falls below the pressure in the aorta. Aortic blood flow quickly reverses back toward the left ventricle, catching the pocket-like cusps of the aortic valve, and is stopped by aortic valve closure. Similarly, as the pressure in the right ventricle falls below the pressure in the pulmonary artery, the pulmonary valve closes. The S2 sound results from reverberation within the blood associated with the sudden block of flow reversal.
Splitting of S2, also known as physiological split, normally occurs during inspiration because the decrease in intrathoracic pressure increases the time needed for pulmonary pressure to exceed that of the right ventricular pressure. A widely split S2 can be associated with several different cardiovascular conditions, including right bundle branch block,pulmonary stenosis, and atrial septal defect.

S3
Rarely, there may be a third heart sound also called a protodiastolic gallop, ventricular gallop, or informally the "Kentucky" gallop as an onomatopoeic reference to the rhythm and stress of S1 followed by S2 and S3 together (S1=Ken; S2=tuck; S3=y).
"lub-dub-ta" or "slosh-ing-in" If new, indicates heart failure or volume overload.
It occurs at the beginning of diastole after S2 and is lower in pitch than S1 or S2 as it is not of valvular origin. The third heart sound is benign in youth, some trained athletes, and sometimes in pregnancy but if it re-emerges later in life it may signal cardiac problems, such as a failing left ventricle as in dilated congestive heart failure (CHF). S3 is thought to be caused by the oscillation of blood back and forth between the walls of the ventricles initiated by blood rushing in from the atria. The reason the third heart sound does not occur until the middle third of diastole is probably that during the early part of diastole, the ventricles are not filled sufficiently to create enough tension for reverberation.
It may also be a result of tensing of the chordae tendineae during rapid filling and expansion of the ventricle. In other words, an S3 heart sound indicates increased volume of blood within the ventricle. An S3 heart sound is best heard with the bell-side of the stethoscope (used for lower frequency sounds). A left-sided S3 is best heard in the left lateral decubitus position and at the apex of the heart, which is normally located in the 5th left intercostal space at the midclavicular line. A right-sided S3 is best heard at the lower-left sternal border. The way to distinguish between a left and right-sided S3 is to observe whether it increases in intensity with inspiration or expiration. A right-sided S3 will increase on inspiration, while a left-sided S3 will increase on expiration.
S4
S4 when audible in an adult is called a presystolic gallop or atrial gallop. This gallop is produced by the sound of blood being forced into a stiff or hypertrophic ventricle.
"ta-lub-dub" or "a-stiff-wall"
It is a sign of a pathologic state, usually a failing or hypertrophic left ventricle, as in systemic hypertension, severe valvular aortic stenosis, and hypertrophic cardiomyopathy. The sound occurs just after atrial contraction at the end of diastole and immediately before S1, producing a rhythm sometimes referred to as the "Tennessee" gallop where S4 represents the "Ten-" syllable. It is best heard at the cardiac apex with the patient in the left lateral decubitus position and holding his breath. The combined presence of S3 and S4 is a quadruple gallop, also known as the "Hello-Goodbye" gallop. At rapid heart rates, S3 and S4 may merge to produce a summation gallop, sometimes referred to as S7.
Atrial contraction must be present for production of an S4. It is absent in atrial fibrillation and in other rhythms in which atrial contraction does not precede ventricular contraction.

The breakdown of EKG
What is an electrocardiogram?
An electrocardiogram (ECG or EKG) is one of the simplest and fastest procedures used to evaluate the heart. Electrodes (small, plastic patches) are placed at certain locations on the chest, arms, and legs. When the electrodes are connected to an ECG machine by lead wires, the electrical activity of the heart is measured, interpreted, and printed out for the doctor's information and further interpretation.
Other related procedures that may be used to assess the heart include exercise electrocardiogram (ECG), Holter monitor, signal-averaged ECG, cardiac catheterization, chest X-ray, computed tomography (CT scan) of the chest, echocardiography, electrophysiological studies, magnetic resonance imaging (MRI) of the heart, myocardial perfusion scans, radionuclide angiography, and cardiac CT scan. Please see these procedures for additional information.

The heart's electrical conduction system
The heart is, in the simplest terms, a pump made up of muscle tissue. The heart's pumping action is regulated by an electrical conduction system that coordinates the contraction of the various chambers of the heart.
An electrical stimulus is generated by the sinus node (also called the sinoatrial node, or SA node), which is a small mass of specialized tissue located in the right atrium (right upper chamber) of the heart.
The sinus node generates an electrical stimulus regularly at 60 to 100 times per minute under normal conditions. This electrical stimulus travels down through the conduction pathways (similar to the way electricity flows through power lines from the power plant to your house) and causes the heart's lower chambers to contract and pump out blood. The right and left atria (the two upper chambers of the heart) are stimulated first and contract a short period of time before the right and left ventricles (the two lower chambers of the heart). | Click image to enlarge |
The electrical impulse travels from the sinus node to the atrioventricular node (also called AV node), where impulses are slowed down for a very short period, then continue down the conduction pathway via the bundle of His into the ventricles. The bundle of His divides into right and left pathways to provide electrical stimulation to the right and left ventricles.
This electrical activity of the heart is measured by an electrocardiogram. By placing electrodes at specific locations on the body (chest, arms, and legs), a graphic representation, or tracing, of the electrical activity can be obtained. Changes in an ECG from the normal tracing may indicate one or more of several heart-related conditions.

Understanding ECG tracings
Almost everyone knows what a basic ECG tracing looks like. But what does it mean?
The first short upward notch of the ECG tracing is called the "P wave." The P wave indicates that the atria (the two upper chambers of the heart) are contracting to pump out blood.
The next part of the tracing is a short downward section connected to a tall upward section. This next part is called the "QRS complex." This part indicates that the ventricles (the two lower chambers of the heart) are contracting to pump out blood.
The PR interval corresponds to the time measured from the beginning of the P wave to the beginning of the R (or Q) wave. The PR interval indicates the amount of time the electrical impulses take to reach the ventricles from the sinus node.
The next short upward segment is called the "ST segment." The ST segment indicates the amount of time from the end of the contraction of the ventricles to the beginning of the rest period before the ventricles begin to contract for the next beat.
The next upward curve is called the "T wave." The T wave indicates the resting period of the ventricles.
When the doctor views an ECG, he or she studies the size and length of each part of the ECG. Variations in size and length of the different parts of the tracing may be significant. The tracing for each lead of a 12-lead ECG will look different, but will have the same basic components as described above. Each lead of the 12-lead ECG is "looking" at a specific part of the heart, so variations in a lead may indicate a problem with the part of the heart associated with a particular lead.

Parts of the ECG explained

P-waves
P-waves represent atrial depolarisation
In sinus rhythm, there should be a P-wave preceding each QRS complex PR interval
The PR-interval is from the start of the P-wave to the start of the Q wave
It represents the time taken for electrical activity to move between the atria and ventricles

QRS complex
The QRS-complex represents depolarisation of the ventricles
It is seen as 3 closely related waves on the ECG (Q,R & S wave);
ST segment
The ST-segment starts at the end of the S-wave & finishes at the start of the T-wave
It represents ventricular repolarisation T-wave
The T-wave represents ventricular re-polarisation
It is seen as a small wave after the QRS complex RR-interval
The RR-interval starts at the peak of one R wave to the peak of the next R wave
It represents the time between two QRS complexes QT-interval
The QT-interval starts at the beginning of the QRS complex and finishes at the end of the T-wave
It represents the time taken for the ventricles to depolarise & then repolarise

Compare and contrast the two different types of heart failure
The two main types of heart failure are chronic heart failure and acute heart failure .
Chronic heart failure is more common and symptoms appear slowly over time and worsen gradually.
Acute heart failure develops suddenly and symptoms are initially severe. Acute heart failure either follows a heart attack that has caused damage to an area of your heart or, more frequently, is caused by a sudden lack of ability by the body to compensate for chronic heart failure.
If you develop acute heart failure, it may be severe initially but may only last for a brief time and improve rapidly. It usually requires therapy and administration of medication by injection (intravenously).
There is another type of heart failure: Heart failure of the right ventricle.
Heart failure usually results from damage to the main pumping chamber, the left ventricle, which supplies the body with blood. This may be due to muscle injury such as a heart attack or damage to the valves in the left side of the heart.This causes congestion in the lungs and shortness of breath.Sometimes, heart failure mainly affects the right ventricle which pumps blood to the lungs. This may be due to muscle injury, such as a heart attack localized to the right ventricle or damage to the valves in the right side of the heart.This may cause congestion in the liver, intestines and fluid accumulation in the lower limbs.Heart failure on both sides of the heart may be caused or worsened by irregular heart rhythms such as atrial fibrillation, which is usually a rapid and irregular heart rate that may prevent proper filling of the ventricles.
Heart failure symptoms can vary widely from person to person, depending on the type of heart failure you have. Therefore, you may experience all of the symptoms described here or just a few of them. in the early stage, you are unlikely to notice any symptoms, but if your heart failure progresses you are likely to experience symptoms, which become more severe.
The main symptoms of heart failure re caused by fluid accumulation or congestion. and poor blood flow to the body. This section will explain these symptoms and provide tips on how to improve them.
Differentiate between anemia and iron deficiency anemia
What is iron deficiency?
Iron deficiency is a condition resulting from too little iron in the body. Iron deficiency is the most common nutritional deficiency and the leading cause of anemia in the world. In the USA, despite food fortification, iron deficiency is on the rise in certain populations.

Iron deficiency at critical times of growth and development can result in premature births, low birth weight babies, delayed growth and development, delayed normal infant activity and movement. Iron deficiency can result in poor memory or poor cognitive skills (mental function) and can result in poor performance in school, work,and in military or recreational activities. Lower IQs have been linked to iron deficiency occurring during critical periods of growth.
Signs and symptoms of iron deficiency
A person who is iron deficient may also be anemic and as a result may have one or more symptoms of anemia. These can include, chronic fatigue, weakness, dizziness, headaches, depression, sore tongue, sensitivity to cold (low body temp), shortness of breath doing simple tasks (climbing stairs, walking short distances, doing housework), restless legs syndrome, pica (the desire to chew ice or non-food items,) and loss of interest in work, recreation, relationships, and intimacy.
Causes iron deficiency
Iron deficiency can be the result of numerous and multiple causes. These fall into two broad categories: an increased need for iron and/or decreased intake or absorption of iron.

If you have anemia, your blood does not carry enough oxygen to the rest of your body. The most common cause of anemia is not having enough iron. Your body needs iron to make hemoglobin. Hemoglobin is an iron-rich protein that gives the red color to blood. It carries oxygen from the lungs to the rest of the body.
Anemia has three main causes: blood loss, lack of red blood cell production, and high rates of red blood cell destruction.
Conditions that may lead to anemia include * Heavy periods * Pregnancy * Ulcers * Colon polyps or colon cancer * Inherited disorders * A diet that does not have enough iron, folic acid or vitamin B12 * Blood disorders such as sickle cell anemia and thalassemia, or cancer * Aplastic anemia, a condition that can be inherited or acquired * G6PD deficiency, a metabolic disorder

Anemia can make you feel tired, cold, dizzy, and irritable. You may be short of breath or have a headache. Anemia is the most common disorder of the blood with it affecting about a quarter of people globally. Iron-deficiency anemia affects nearly 1 billion.

Sickell Cell Disease
Sickle cell disease is the most common of the hereditary blood disorders. It occurs almost exclusively among black Americans and black Africans.
Sickle cell disease in black Americans occurs in about 1 in 500 live births.
The first account of what was then called sickle cell anemia in the medical literature was in 1910. James B. Herrick, a Chicago physician, described the symptoms of a 20-year-old black male student from the West Indies. The man had reported "shortness of breath, palpitations, and episodes oficterus [yellow eyes]. He had an anemia." Dr. Herrick described the patient's blood smear as showing "thin, sickle-shaped and crescent-shaped red cells."
Red blood cells deliver oxygen to working or active tissues. In the lungs,hemoglobin (the molecule in the red blood cell) takes on oxygen and, at the same time, releases carbon dioxide. This process is called oxygenation. At the tissue level, this activity is reversed. The same hemoglobin molecule releases oxygen and takes on carbon dioxide. This process is called deoxygenation.
In sickle cell disease, certain red blood cells become crescent-shaped (the sickle cell Dr. Herrick described). These abnormal red blood cells, carrying an abnormal hemoglobin known as hemoglobin S, are fragile. A person who has sickle cell disease can become more likely to get infections because the damaged cells eventually clog the spleen. A severe attack, known as sickle cell crisis, can cause pain because blood vessels can become blocked or the defective red blood cells can damage organs in the body. There is also an impairment in oxygentation from the abnormal hemoglobin S.
Sickle cell disease results from mutation, or change, of certain types of hemoglobin chains in red blood cells (the beta hemoglobin chains).

The changes in the building of normal hemoglobin result in the abnormal hemoglobin of sickle cell disease. These mutated molecules do not have the smooth motion needed for oxygenation and deoxygenation. When the oxygenconcentration in the blood is reduced, the red blood cell assumes the characteristic sickle shape. This causes the red blood cell to be stiff and rigid, and stops the smooth passage of the red blood cells through the narrow blood vessels.

Sickle Cell Disease Treatment at Home
Even tiny changes in the red blood cells can begin a cascade of symptoms leading to a sickle cell crisis. Therefore, home care, even when a person is careful about drinking plenty of fluids and avoiding infection, is difficult. The best home care is understanding the illness and knowing when and where to seek immediate medical care.
Sickle Cell Treatment with Medications
Sickle cell pain crisis * Pain medications, often narcotics, will be given. * IV fluids are an important part of therapy. * Infection: If the physician diagnoses or suspects a bacterial infection, antibiotics are prescribed. * Anemia: If there is a significant decrease in the red blood cell count, a red blood cell transfusion may be needed. * Hydroxyurea may be used to increase the amount of Hgb F and decrease the amount of Hgb S, which can decrease the long-term risks of sickle cell crises.
Other Therapy for Sickle Cell Disease
Chronic therapy: New developments in regularly scheduled transfusion therapy have shown promise in decreasing the following: * Symptoms of acute chest syndrome * Incidence of stroke * Severity of pain crises * Bone marrow transplantation holds promise for a very small percentage of people with sickle cell disease. Discuss this with the physician.

Sickle Cell Disease Follow-up
Considering the many body systems involved and the likelihood that sickle cell crisis will occur time and time again, strong consideration should be given to follow-up with a hematologist (a physician with a specialty in treating blood disorders).
Most uncomplicated cases of sickle cell crisis can be treated in community emergency departments. People with this condition can be safely sent home when their pain is under control and their dehydration is eliminated. A short observational period in the emergency department helps to prevent acute relapse and admission for pain and rehydration.

Blood types

There are 4 major blood groups determined by the presence or absence of two antigens (A and B) on the surface of red blood cells:

Blood Group | Antigen | A | Has only A antigen on red cells (and B antibody in the plasma) | B | Has only B antigen on red cells (and A antibody in the plasma) | AB | Has both A and B antigens on red cells (but neither A nor B antibody in the plasma) | O | Has neither A nor B antigens on red cells (but both A and B antibody are in the plasma) |

In addition to the A and B antigens, there is a third antigen called the Rh factor, which can be either present (+) or absent ( - ). In general, Rh negative blood is given to Rh-negative patients, and Rh positive blood or Rh negative blood may be given to Rh positive patients. * The universal red cell donor has Type O negative blood type. * The universal plasma donor has Type AB positive blood type.

What Does Blood Group RH Factor Mean
RH factor in blood types stands for "Rhesus Factor". Blood tests were performed on Rhesus monkeys and the Rh+ and Rh- factors were isolated. An antigen found in the red blood cells of most people: those who have Rh factor are said to be Rh positive (Rh+), while those who do not are Rh negative (Rh-). What about the meaning of RHD- Rh blood group, D antigen. The rhesus complex is not just one antigen, but several, when someone is told to be Rh+, it usually refers to the D antigen (one of the components of the Rh complex), because it's the most common, and the easiest to identify, however it's not the only one.
What is the Rarest Blood Type
According to the American Red Cross the rarest is AB(-), present in 1% of the Caucasians, in African Americans it is even rarer. B(-) and O(-) are also very rare, each accounting for less than 5% of the world's population. Some people with rare blood types bank their own blood in advance of surgical procedures to ensure that blood is available to them.
Rh incompatibility

Rh incompatibility is a condition that develops when a pregnant woman has Rh-negative blood and the baby in her womb has Rh-positive blood.
Causes
During pregnancy, red blood cells from the unborn baby can cross into the mother's bloodstream through the placenta.
If the mother is Rh-negative, her immune system treats Rh-positive fetal cells as if they were a foreign substance and makes antibodies against the fetal blood cells. These anti-Rh antibodies may cross back through the placenta into the developing baby and destroy the baby's circulating red blood cells.
When red blood cells are broken down, they make bilirubin. This causes an infant to become yellow (jaundiced). The level of bilirubin in the infant's bloodstream may range from mild to dangerously high.
Because it takes time for the mother to develop antibodies, firstborn infants are often not affected unless the mother had past miscarriages or abortions that sensitized her immune system. However, all children she has afterwards who are also Rh-positive may be affected.
Rh incompatibility develops only when the mother is Rh-negative and the infant is Rh-positive. Thanks to the use of special immune globulins called RhoGHAM, this problem has become uncommon in places that provide access to good prenatal care.

Treatment

Because Rh incompatibility is preventable with the use of RhoGAM, prevention remains the best treatment. Treatment of an infant who is already affected depends on the severity of the condition.
Infants with mild Rh incompatibility may be treated with phototherapy using bilirubin lights. IV immune globulin may be used, but there is no conclusive evidence to show it works