BIOS 3455 Exam 2
What are antigens?
*Antigens* are chemical substances, which when introduced into an animal will stimulate the animal's immune system to produce *antibodies*. Each lymphocyte is capable of attacking a specific antigen, which can bond to a specific receptor protein on the outer membrane of the lymphocyte. By means of this bonding, the antigen inadvertently selects the lymphocyte capable of attacking it. When bonding of the antigen occurs, the T-lymphocyte is stimulated to divide many times until a large population of genetically identical cells (clones) is produced. This clone selection theory accounts for the fact that the immune response to all following exposures to an antigen is greater than the immune response to the initial antigen exposure. In general T-lymphocytes have their effect on abnormal body cells (virus-infected or cancer).
What is blood type O?
.Neither A nor B antigen; plasma contains both anti-A and anti-B antibodies.
What is the function and WBC percentage of basophils?
0.5% Inflammatory response
What is blood type A?
A antigen on its red cell membranes; plasma contains anti-B antibodies.
What are diseases of blood cells?
A condition known as *erythrocytopenia* exists when there is a decrease in the circulating number of red blood cells below the normal range. This condition is seen in many types of anemia. When red blood cells exist in numbers greater than the normal range, it constitutes a condition known as *polycythemia*.
What is thrombocytopenia?
A decrease in the circulating number of platelets is called *thrombocytopenia*. This condition is usually not critical unless the platelet count is below 50,000 per cubic millimeter. At this point, bleeding may result from minor trauma. Bleeding may occur spontaneously if the platelet count is 20,000 per cubic millimeters or less. Thrombocytopenia may be caused by decreased activity of the bone marrow (resulting in decreased number of megakaryocytes), excessive destruction of platelets, or a disturbance in formation of platelets.
What is the Bainbridge reflex?
A very common arrhythmia occurs in conjunction with respiration. During inspiration the large veins in the thoracic cavity fill with blood and during expiration this blood is forced into the heart. If there is an increase in filling there will be an increase in heart rate, this is called the *Bainbridge reflex*. Therefore heart rate frequently increases and decreases during the respiratory cycle and is referred to as a *sinus arrhythmia*.
What is vascular spasm?
After a blood vessel is cut or ruptured, the immediate response is constriction of its walls to reduce the amount of bleeding (vascular spasm). This constriction has been attributed to the following: 1) local spasms of the smooth muscle in the vessel's wall, 2) sympathetically mediated constriction, and 3) platelet release of vasoconstrictor substances, such as *serotonin*. This vasoconstriction not only reduces the blood flow from the vessel but also promotes platelet aggregation at the site and the accumulation of substances that assist in coagulation (process of clotting).
What is the corrected hematocrit?
After centrifuging the blood, a certain amount of plasma always remains trapped among the red cells. It has been found that approximately 4 percent of the plasma remains in the red cell packed layer. To obtain a *corrected hematocrit*, the value of the apparent hematocrit is multiplied by 0.96 (unless otherwise indicated, you can assume that reported hematocrit values have already been corrected). In severe *anemia* the hematocrit may fall to as low as 15% and individuals with *polycythemia* may have a hematocrit as high as 70%.
What is the first Korotkoff sound?
Appearance of a fairly sharp thudding sound that increases in intensity during the next 10 mmHg decrease in pressure. The pressure when the sound first appears is the systolic pressure.
What is blood type B?
B antigen on its red cell membranes; plasma contains anti-A antibodies.
What variables most affect SBP and DBP?
Because the SBP is the peak arterial pressure during ventricular systole,* it is especially dependent upon the stroke volume and cardiac output*. Recall that systole is contraction of the ventricle and the SV is the result of this contraction. During diastole, blood is not being pumped out of the left ventricle into the arterial circulation. Thus, the DBP is especially affected by the *resistance of the blood vessels* (i.e. the resistance is what keeps the arterial pressure from falling to 0 mmHg when blood is not being ejected into the arterial circulation). However, stroke volume and cardiac output do influence the DBP, and resistance does affect the SBP.
What are leukocytes?
Because they do not contain a colored pigment, leukocutes do not actually appear white but transluscent or colorless in an unstained preparation for light microscopes. All leukocytes contain a nucleus. All leukocytes develop in the red bone marrow but differ in their appearance. White blood cells are categorized according to the appearance of their cytoplasm: 1) *granulocytes*, whose cytoplasm contains a large number of granules, and 2) *agranulocytes*, whose cytoplasm appears relatively free of granules.
How does blood flow through the body?
Blood flow through the heart and circulatory system is as follows: Superior and Inferior Vena Cava -> Right Atrium -> Tricuspid Valve -> Right Ventricle -> Pulmonic Semilunar Valve -> Pulmonary Artery -> Lungs (capillaries) -> Pulmonary Veins -> Left Atrium -> Mitral Valve -> Left Ventricle -> Aortic Semilunar Valve -> Aorta -> Systemic Arterial Vessels -> Systemic Capillaries -> Systemic Venous Vessels -> Vena Cava
What are the effects of gravity on blood pressure?
Blood pressure is usually measured at or near the level of the heart- (one reason the arm is so often used for blood pressure measurements). This is because gravity has an effect on blood pressure. The pressure in any artery below the heart is higher than the pressure at the level of the heart, while that pressure in any artery above the level of the heart is lower than the pressure at heart level. At the density of normal blood, this pressure difference is 0.77mmHg per centimeter distance from the heart. Examples: In an upright position, when the mean arterial pressure at heart level is 100mmHg, the mean pressure in a large artery in the head (50 cm above the heart) is 62 mmHg: (100 - [0.77 X 50] = 62) and the pressure in a large artery in the foot (105 cm below the heart) is 180 mmHg: (100 + [0.77 X 105] = 180).
What is blood and why is it important?
Blood provides a medium for the maintenance of homeostasis in the cell's environment
How can bloodborne pathogens be transmitted?
Bloodborne pathogens can be transmitted through contact with infected human blood and other potentially infectious body fluids such as: semen, vaginal secretions, cerebrospinal fluid, synovial fluid, pleural fluid, peritoneal fluid, amniotic fluid, saliva, and any body fluid that is visibly contaminated with blood. Anytime there is blood-to-blood contact with infected blood or body fluids, there is a slight potential for transmission. Unbroken skin forms an impervious barrier against bloodborne pathogens. However, infected blood can enter your system through: open sores, cuts, acne, abrasions, any sort of damaged or broken skin such as sunburn or blisters, mucous membranes.
What is blood type AB?
Both A and B antigens on red cells membranes; plasma lacks both anti-A and anti-B antibodies.
Can the autonomic nervous system affect AV node conduction?
Both the sympathetic and parasympathetic nervous system can alter AV node conduction velocity to some extent. The parasympathetic nervous system does not innervate the ventricular myocardium, thus only the sympathetic nervous system directly influences ventricular contractility under normal circumstances.
What mechanisms regulate arterial pressure?
By far, the most rapid controls are the nervous pressure control mechanisms. Both branches of the autonomic nervous system affected blood pressure. An increase in *sympathetic nervous system* activity is usually associated with an increase in blood pressure by increasing cardiac output and/or by causing vasoconstriction of blood vessels. On the other hand if blood pressure is too high, and needs to be lowered, a decrease in sympathetic nervous system activity occurs and there is a concomitant activation of the *parasympathetic nervous system*, which decreases heart rate.
What other mechanisms respond to changes in arterial pressure?
Three other mechanisms respond within minutes of pressure change. These are: 1) the *renin-angiotensin-aldosterone system*, 2) *stress relaxation* changes in vasculature, and 3) a fluid shift through the capillaries from the tissues into or out of the circulation to readjust *blood volume*. The long term regulation rests mainly on a *renal-body fluid-pressure control mechanism*. A portion of this mechanism involves hormonal control of kidney function, including the renin-angiotensin-adosterone system.
What is relaxation time?
Time from peak tension until tension decreased to zero.
What is leukopenia?
Conditions involving circulating white blood cells in numbers below the lower limit of the normal range are known as *leukopenia*. Causes for leukopenia include certain ifnections and depression of bone marrow production due to radiation, poisoning, or alcoholism.
What is functional syncytium?
Due to the presence of *gap junctions*, specialized proteins located in the *intercalated discs* between cardiac muscle cells, once one cell in the heart reaches threshold a wave of depolarization and repolarization will spread from cell to cell through the entire myocardium. This arrangement allows the heart to function collectively. However, the heart contains a fibrous skeleton, which separates the upper atria from the lower ventricles.
What is EKG paper?
EKGs are usually recorded on a standardized *EKG paper* resembling graph paper with red lines. On EKG paper, each of the vertical thick red lines is separated from each other by a horizontal distance of 5 mm and represents a time of 0.2 seconds. Each thin red line is separated by a horizontal distance of 1 mm and represents 0.04 seconds. Thus, the PR interval, which is usually 0.12 to 0.2 seconds long, is usually 3 to 5 "small boxes" across and the QRS interval (0.08 to 0.12 seconds normally) is 2-3 "small boxes" across. A vertical distance of 10 mm usually represents a deflection of 1 mV on a standard EKG tracing.
What happens during the later stages of ventricular diastole?
Here, the *mitral* and *tricuspid valves* between the atria and ventricles are open and the aortic and pulmonary valves are closed. As blood flows into the heart, throughout diastole, the atria and ventricles fill. The rate of ventricular filling decreases as the ventricles become distended. The cusps of the *atrioventricular (AV) valves* also begin to drift towards the closed position and pressure in the ventricles remains low. As the atria contract, additional blood is pumped into the ventricles. However, about 70-80% of *ventricular filling* occurs passively during diastole. During atrial systole, there is some regurgitation of blood into the vena cava and pulmonary veins, but the narrowing of their orifices and the inertia of blood flow assist in keeping the blood in the atria.
Which blood cells are not true cells?
Erythrocytes and thrombocytes are not true cells by definition because they lack nuclei and are incapable of undergoing mitosis to form daughter cells. Because of these characteristics, they act as chemical-containing membrane-bound "bags"--the erythrocytes carrying mostly hemoglobin and the thrombocytes carrying a variety of factors related to hemostasis.
What are bundle branch blocks on an EKG?
Example of a *conduction system block* QRS complexes are >0.12 seconds in duration We often see R-R' QRS complexes in some leads
What is a second degree AV block on an EKG?
Example of a *conduction system block* PR interval is progressively lengthening, and eventually a QRS complex is dropped
What is a third degree AV block on an EKG?
Example of a *conduction system block* There is absolutely no association between P waves and QRS complexes
What is ventricular fibrillation on an EKG?
Example of an *abnormal conduction pathway* No discernable P waves No discernable QRS complexes "Bag of worms: Is really bad
What is a multifocal premature ventricular contraction on an EKG?
Examples of *ectopic foci* Are premature QRS complexes are >0.12 seconds No P wave precedes the bizarre QRS complex Because they come from different ectopic foci they are different shapes
What is a unifocal premature ventricular contraction on an EKG?
Examples of *ectopic foci* Are premature QRS complexes are > 0.12 seconds No P wave precedes the bizarre QRS complex Because they come from the same ectopic focus-they are the same shape
What is load?
Force exerted on a muscle by the weight of an object.
What is the formula for a hematocrit?
Hct (%) =( height of red cells (mm)/ height of red cells and plasma) X 100
What is sinus bradycardia on an EKG?
Heart rate < 60 bpm T waves > P waves Increasing R-R interval
What is sinus tachycardia on an EKG?
Heart rate > 100 bpm
What is sinus arrhythmia?
Individuals with *sinus arrhythmia* have an RR interval that varies with the respiratory cycle. Thus, it is necessary to measure the RR interval several places across the EKG.
What are the two types of protein myofilaments found inside each myofibril?
Inside each myofibril are two types of protein myofilaments; the *thick myosin filament* and the *thin actin filament*. The thick filaments are centrally located in the sarcomere and are responsible for the dark appearance of the A band. The thick filaments are primarily composed of *myosin*. The thick filaments are held in place by a large, elastic protein named *titin*, which extends from each side of the thick filament to the Z line. The thin filaments are attached to each Z line and extend towards the middle of the sarcomere. The thin filaments are made up primarily of *actin*, *troponin*, and *tropomyosin*. The actin and the myosin partially overlap in the A band region and give the A band a darker appearance. The I band, on the other hand, is lighter because it has no thick filaments. The *H zone* is the central region of the Z band where there are no thin filaments.
What is sinus arrhythmia on an EKG?
Is an example of *abnormal pacemaker function* HR varies with respiration, usually increases during inspiration and decreases during expiration (look at R-R intervals) SA node is still pacemakerr Normal P waves This is really quite common in young people; i.e. it is not that "abnormal"
What is a first degree AV block on an EKG?
Is an example of a *conduction system block* PR interval is > 0.20 seconds long
What is atrial fibrillation on an EKG?
Is an example of an *abnormal conduction pathway* No discernible P waves "Bag of worms" isoelectric line RR interval is variable
What is oxygen carrying capacity?
Hemoglobin concentration is the primary determinant of the *oxygen carrying capacity*. The oxygen carrying capacity of normal blood is approximately 20 mL/dL (mL oxygen per 100 mL blood, also called *volumes percent*, abbreviated *vols %*). Each gram of hemoglobin can maximally carry 1.39 mL of oxygen (the oxygen carrying capacity of hemoglobin). Thus, if you know your subject's hemoglobin concentration you can calculate their oxygen carrying capacity. For example if their hemoglobin concentration is 14.5 g/dL then their oxygen carrying capacity is 14.5 g/dL X 1.9 mL O2/g = 20.2% vols. Normal adult ranges for oxygen carrying capacity are *18.0-22.9 vols% for males* and *16.2-20.3 vols% for females*. A low oxygen carrying capacity of blood (below 13.5 mL/dL) is a key sign of *anemia*. Anemia can be the result of a low number of circulating red blood cells and/or a lower hemoglobin content (<10 g/dL). Due to reduced oxygen carrying capacity, physical signs of anemia can include physical weakness, shortness of breath, heart palpitation, and difficult in doing mental tasks.
What affects hemoglobin concentration?
Hemoglobin concentrations vary depending on a number of variables, including: age, developmental status, physical activity status, exposure to altitude, various diseases, or loss of plasma. For example, newborns have a hemoglobin concentration of approximately 24 g/dL. By 1-2 years of age, the concentration level decreases to approximately 11.5 g/dL. By 16 years of age, normal adult hemoglobin concentrations are obtained.
What is hemoglobin?
Hemoglobin is a respiratory pigment in red blood cells that readily associates and dissociates with oxygen and carbon dioxide. Hemoglobin (Hb) is composed of two parts, an iron-containing *heme* group and a *globin* portion. The globin portion is made up of four subunit polypeptide chains and each is attached to a heme group. Because of its central ferrous ion, each heme group can bind with a molecule of oxygen, and therefore, a molecule of hemoglobin can combine with four oxygen molecules (*oxyhemoglobin*). Binding of carbon dioxide to hemoglobin on the globin portion of the molecule results in the formation of *carbinohemoglobin*. Hemoglobin has the ability to transport both oxygen and carbon dioxide at the same time. When hemoglobin is saturated with oxygen, blood has a bright red color. Hemoglobin that gives up oxygen is known as *reduced hemoglobin*. In the reduced state, the hemoglobin gives blood a blue-purple color. The primary function of hemoglobin is to enable red blood cells to carry oxygen from the lungs to the body tissues, and to transport carbon dioxide from the body tissues to the lungs. Hemoglobin also functions as a chemical buffer in the body's defense against pH (hydrogen ion concentration) changes.
How is unidirectional flow maintained?
Unidirectional flow is maintained by the cardiac valves. Two *atrioventricular (AV) valves* separate the atria and the ventricles. The right AV valve or *tricuspid valve* and the left AV valve or mitral (*bicuspid*) valve have valve flaps called cusps that have thread-like *chordae tendinae* attached to theri edges. These chordae tendinae connect the cusps to *papillary muscles* located on the ventricular walls. Because of these connections, the valves can normally open in one direction. the two *semilunar valves*, the *aortic and pulmonic*, each have three cusps attached to the walls of their respective arterial trunks. These four valves are anchored to four fibrous rings that are referred to as the *fibrous skeleton* of the heart.
What is a 12-lead EKG?
Utilizing these concepts and placing surface electrodes on standard areas of the body we can produce standard lead configuration with reproducible waveforms. The placement of electrodes in different arrangements allows for different views of the same electrical event. Some leads provide better information than others regarding a specific area of the heart. For this reason several lead combinations are frequently used to give a comprehensive evaluation of the electrical activity of the heart. A *12 lead EKG* is a standard procedure that uses the combination of 10 different electrodes to provide 12 different lead configurations. A standard 12 lead EKG includes: three *limb leads*, three *augmented voltage leads*, and six *precordial leads*.
What happens when B-lymphocytes are stimulated by antigens?
When B-lymphocytes are stimulated by antigens, they develop into plasma cells that secrete significant amounts of antibody into the plasma. This may destroy the bacteria in one of two ways: 1) the antibodies coat the bacterial cell, making it more susceptible to phagocytic neutrophils and tissue macrophages; 2) attaching antibodies to antigen on the bacterial surface activates a system of plasma proteins which lyse the bacterial cell. These two systems work together, since a chemical release from the system of plasma proteins (complement system) attracts the phagocytic leukocytes and increases capillary permeability.
What is a combined white blood cell count?
When leukocytes are counted regardless of type, the count is termed a *combined white blood cell count*. In some circumstances, it is helpful to the number of white blood cells according to type. This count is known as a *differential white blood cell count*.
Which bands shorten during muscle contraction?
When the muscles shorten during a contraction, the I band and H zone get shorter as actin and myosin "slide" over each other. The A band whose thick filaments make it appear dark, does not shorten during contraction because the thick filaments do not change in length.
What is the myofibril?
Within the muscle fiber are smaller parallel strands of protein known as *myofibrils*. The myofibril has a regular banding pattern which gives the muscle fiber its striated appearance. Between two lighter *I bands* is a darker *A band*. In the middle of each I band is a dark *Z line*. The segment between two adjacent Z-lines is called a *sarcomere*. The myofibrils are surrounded by the cell's cytoplasm known as *sarcoplasm*. Forming a continuous membranous structure of tubules and vesicles around the myofibrils is the *sarcoplasmic reticulum*. The sarcoplasmic reticulum is a muscle cell's endoplasmic reticulum and it has a repetition of structure within each sarcomere.
What is the conduction system?
Within the myocardium is specialized muscle tissue that exhibits very rapid conduction ability. This tissue is arranged in such a way to allow the impulse to be rapidly distributed to different parts of the heart at different times. This system is responsible for the order and timing of the electrical (and contraction) events within the heart. *Sino-atrial node* (SA), *internodal* and *interatrial tracts*, *atrioventricular node* (AV), the *common AV bundle* (of His), *right and left bundle branches* and the *Purkinje fibers*.
What is a premature atrial contraction on an EKG?
Won't be tested
What are the four categories of arrhythmias?
a) Abnormal pacemaker function -Sinus arrhythmia b) Ectopic focus -PACs, PVCs c) Conduction system blocks -Atrioventricular (1st, 2nd, and 3rd degree) and bundle branch blocks d) Abnormal conduction pathways -Flutter and fibrillation pathways
What are the methods for determining heart rate?
a) Count the number of small boxes for one RR interval and multiply that number by 0.04 seconds. Then divide 60 by that number. b) Count the number of small boxes for one RR interval and use the following formula: 1500/#small boxes = heart rate.
What is arterial oxygen content?
It is important to note that hemoglobin in our arterial circulation is not always 100% saturated with oxygen, although it is close. In humans, the pO2 in arterial blood is 100mmHg. At this pO2 hemoglobin is usually 98% saturated. Thus if your subject's oxygen carrying capacity is 20.2% vols then they are actually carrying 19.8% vols (20.2 vols% X 0.98) of oxygen in their arterial blood, this is their *arterial oxygen content*. The percent saturation of hemoglobin with oxygen can be determined using a device called a *pulse oximeter*.
What is diapedesis?
Leukocytes can enter connective tissues of the body by squeezing through the capillaries (known as *diapedesis*). During an inflammation response, the permeability of the capillaries for diapedesis is increased by the release of histamine from tissue mast cells and basophils. This process also produces the local edema, redness, and pain associated with inflammation.
What are limb leads I, II and III (as used in our lab)?
Limb Lead I: (+) left arm, (-) right arm Limb Lead II: (+) left leg, (-) right arm Limb Lead III: (+) left leg, (-) left arm Note: for all, right leg is ground (See page 11)
What is parasympathetic stimulation of the heart?
Neurotransmitter: Acetylcholine Receptors involved: Muscarinic G Protein: Gi (inhibits AC) cAMP: Decrease Membrane permeability: More to K+, Less to Ca2+ SA Node: Decreases HR AV Node: Increases AV Nodal Delay Ventricular Conduction Pathway: --- Atrial Muscle: Decrease in contractility (*indirect may increase) Ventricular Muscle: --- Adrenal Medulla: --- Receptor Antagonist: Atropine
What is sympathetic stimulation of the heart?
Neurotransmitter: Norepinephrine Receptors involved: Beta-1 adrenergic G Protein: Gs (stimulates adenylyl cyclase) cAMP: Increase Membrane Permeability: Less to K+, More to Ca2+ SA Node: Increases HR AV Node: Decreases AV Nodal Delay Ventricular Conduction Pathway: Increased conduction through bundles and Purkinje cells Atrial Muscle: Increase in contractility (*indirect may decrease contractility) Ventricular Muscle: Increased contractility* Adrenal Medulla: Promotes secretion of epinephrine, which augments SNS actions on the heart Receptor antagonist: Beta-1 blockers/antagonists
What are the heart sounds?
One can listen to and study the various sounds arising from the heart as it pumps blood. This is known as auscultation. These sounds are produced by the vibrations created by the heart valves closing and the blood rebounding against the ventricular and arterial walls. The heart sounds may be heard by placing an ear against the chest or by using a stethoscope. There are four major heart sounds associated with both valvulvar movement and the flow of blood within the heart. The first two can be heard without special amplification.
What are sympathetic effects on the heart?
Sympathetic effects are mediated through the release of *norepinephrine* (the adrenal medulla also contributes to these effects through the release of norepinephrine and *epinephrine*) resulting in a *marked increase in heart rate and ventricular contractility.* (strength of contraction). Epinephrine and norepinephrine affect heart rate and contractility by binding with *beta-1-adrenergic receptors* on the cells of the SA node (affecting HR) and ventricular myocardium (affecting contractility). The binding of either epinephrine or norepinephrine with these beta receptors results in an increase in cellular cAMP, which activates an enzyme protein kinase A, which phosphorylates ion channels and thus changes the permeability of the membrane to potassium and calcium. Thus, the mechanism by which epi and norepi influence heart rate are via increasing the calcium and decreasing the potassium permeability of cells in the SA node. This results in an enhanced automaticity (increase in HR) . Furthermore, the increase in calcium entry into the cardiac myocytes results in enhanced contractility (stronger contractions). *Beta-blockers* are used clinically to block these effects.
What are systolic and diastolic blood pressure?
Systolic blood pressure (SBP) is defined as the peak pressure reached during ventricular systole. Diastolic blood pressure (DBP) is the lowest pressure reached during diastole of the ventricle. A normal value for systolic pressure for a 20-year-old man is 120 mmHg and for diastolic pressure, it is 80 mmHg. The arterial pressure is conventionally written as systolic pressure over diastolic pressure (e.g. 120/80).
How is oxygen carrying capacity calculated?
Oxygen carrying capacity can be calculated after the subject's hemoglobin concentration has been determined, providing an estimate of how many milliliters of oxygen can be carried per 100 mL of a person's blood. Each gram of hemoglobin can carry 1.39 mL of oxygen. Oxygen carrying capacity (mL O2/100 mL blood) = Hemoglobin concentration (g Hb/100 mL) X 1.39 mL oxygen per g Hb This number is often expressed as *vols%* (1 vol% = 1 mL/100 mL blood) instead of mL of oxygen per 100 mL of blood.
What are parallel and series elastic elements?
Passive elastic properties of muscle. Some of the components that contribute to the elastic properties of muscle include the tendons, titin, and the connective tissue sheaths of the muscles, fascicles, and fibers (the *epimysium*, *perimysium*, *and endomysium*, which contain some amount of *elastin).
What factors affect peripheral resistance?
Peripheral resistance depends primarily upon the caliber (diameter) of the blood vessels (i.e. vasoconstriction or vasodilation), but it is also affected by the length of the blood vessel and the viscosity of the blood. According to *Ohm's law*: MAP = Q X TPR
What is a hematocrit?
The *hematocrit* is the percent volume of the whole blood that is occupied by formed elements (which are mostly red blood cells). The hematocrit is determined by centrifuging a small blood sample in special hematocrit capillary tubes. The percent of whole blood composed of cells is determined by the height of the red cells in the tube compared with the height of the total column of blood. The average normal values and ranges for both sexes are listed below: Males: Range 40-52% (Average 45%) Females: Range 36-48% (Average 42%) The percentage of whole blood that is not formed elements is plasma. The plasma is 90% water but also contains numerous organic and inorganic substances, including the *plasma proteins*. Plasma proteins are classified as *albumins*, *globulins* and *fibrinogen*, based on their chemical structure and their biochemical functions.
What are thrombocytes?
Platelets are not blood cells but cytoplasmic fragments split from large cells known as *megakaryocytes* found in the bone marrow. These small oval or round discs are 2-4 micrometers in diameter and consist of a dark staining granular portion (*chronomere*), surrounded by a light staining cytoplasmic portion (*hyalomere*). The normal *platelet concentration* in the blood is between 150,000 and 400,00 per cubic millimeter. Platelets are very active structures with a half-life in the body of 8-12 days and play several important roles in hemostasis.
What is isovolumetric ventricular relaxation?
Pressure continues to drop rapidly after the semilunar valves are closed during a period of *isovolumetric ventricular relaxation*. When the ventricular pressure falls below the atrial pressure the relaxation period ends. The ventricles again fill as the AV valves open. Filling is rapid at first and then decreases as the next cardiac contraction approaches.
What are normal blood cell counts?
Red Blood Cells -Males: 4.5-6.0 million/mm^3 -Females: 4.0-5.5 million/mm^3 White Blood Cells -Both sexes: 5,000-10,000/mm^3 Platelets -Both Sexes: 150,000-400,000/mm^3 -Average 250,000/mm^3
What is blood type Rh-?
Rh antigen is absent; plasma may or may not contain anti-Rh antibodies.
What is blood type Rh+?
Rh antigen on red cell membrane plasma lacks anti-Rh antibodies.
How is blood typing accomplished?
Several types of antigens can exist on the surface of the RBC membrane, including some that are weakly antigenic and are a minor concern for transfusion recipients, and others that are strongly antigenic and a major concern in regards to transfusion. Three strongly antigenic substances that may be found in the RBC membrane are named A, B, and Rh antigens. If a person's red cells possess both the A and B antigens, neither antibody (anti-A nor anti-B) is present in the plasma. If the red cells possess neither the A or B antigen, both antibodies are found in the plasma.
What is unique about the nuclei of skeletal muscle fibers?
Skeletal muscle fibers are *multinucleated*, containing many *myonuclei* throughout the length of the muscle fiber. The myonuclei in normal adult muscle fibers lie just below the sarcolemma, allowing the contractile filaments of the myofibrils to run the length of the fiber uninterrupted.
How does mitochondrial content differ in different types of skeletal muscle fiber?
Some skeletal muscle fibers have an abundance of *mitochondria* as well. *Slow twitch* muscle fibers (*type I fibers*) tend to possess a greater mitochondrial volume than *fast twitch* fibers, and thus have a great ability to use aerobic metabolism. However, the more oxidative fast twitch fibers (*type IIA fibers*) can still possess relatively large volumes of mitochondria if the subject participates in regular physical activity. *Type IIX fibers* tend to have very small mitochondrial volumes, and thus rely heavily on anaerobic glycolysis. Muscle fibers that have a great ability to create ATP aerobically (e.g. Type I fibers and type IIA fibers) usually have great endurance and can avoid fatigue longer than muscle fibers that possess little mitochondria (type IIX) fibers. The more aerobic fibers usually also possess more *capillaries* and more myoglobin.
What are the consequences of incorrect blood typing?
Sometimes when the blood from different people is mixed, the result is agglutination, a clumping of red blood cells. These clumped cells may travel and become lodged in the vasculature, causing malfunction of the organ (e.g. kidney, brain, heart, skeletal muscle) in which it is lodged. Incompatibilities of blood are caused by the presence of antigens on the surface of red blood cell membranes.
What is the mean electrical axis?
The *mean electrical axis* (the average direction of the wave of depolarization) of the heart is from the base toward the apex (down and to the left side of the subject). The mean electrical axis gives us a relative indicator of the direction and magnitude of the electrical activity in the heart. Remember that in a normal human heart as the electrical impulse goes from the SA node to the AV node to the common bundle to the right and left bundle branches to the Purkinje fibers and then into the ventricular myocardium the wave of depolarization tends to go from the right atrium towards the apex of the heart.
What is the rate pressure product?
The *rate pressure product* is a way of estimating the myocardial oxygen demand, and is calculated as HR X SBP. If the heart is beating more frequently or more forcefully, then it makes sense that it requires more oxygen. RPP = HR X SBP
What is the J point?
The J point is the end of the QRS complex and the beginning of the ST segment.
What is the P wave?
The P wave represents depolarization of the myocardial cells in the atria, initiated by the SA node.
What is the QRS complex?
The QRS complex represents depolarization of the myocardial cells in the ventricles. This also happens to coincide with the part of the cardiac cycle when the myocardial cells in the atria are repolarizing. The impulse is slightly delayed at the AV node before entering the ventricles through the common AV bundle.
What is the R-R interval?
The RR interval represents the amount of time between heart beats. Thus, the RR interval is heart rate dependent. When heart rate increases, RR interval decreases and the opposite is true when heart rate decreases. In fact, most of our methods for determining *heart rate* from the EKG are dependent on measuring the RR interval. The RR interval is measured from the peak of one QRS complex (R wave) to the peak of the next QRS complex. If there are 0.6 seconds between beats and there are 60 seconds per minute, then the heart rate would be 100 beats per minute (60 seconds per minute/0.6 seconds per beat).
What is the ST segment?
The ST segment is the segment between the J point (the end of the QRS complex) and the beginning of the T wave. If this segment is significantly below the isoelectric line is is called *ST segment depression* and it suggests that part of the subject's myocardium is not getting enough oxygen (*myocardial ischemia*). This segment is also frequently elevated (*ST segment elevation*) above the isoelectric line in the early stages of a *myocardial infarction*.
What is the T wave?
The T wave represents repolarization of the myocardial cells in the ventricles.
What is the Tallquist method?
The Tallquist method uses a book of special Tallquist blotting papers and a color comparison chart having different intensities of red. These intensities correspond to different concentrations of hemoglobin found in human blood.
What is Starling's Law of the Heart?
The length of the cardiac muscle fiber is increased by an increase in diastolic filling of the heart. This property of cardiac muscle allows the heart to vary its contractile strength depending on the venous return.
What is Einthoven's triangle?
The limb lead configuration is based on *Einthoven's triangle*. This triangle surrounds the heart and is made up of three electrodes placed on the right and left arm and the left leg (an electrode is also placed on the right leg to serve as a ground wire). Combinations of these three electrodes can be used to produce six different views of the heart in the frontal plane.
What is the sliding filament theory?
The major theory used to explain how "contraction" of the muscle occurs is called the *sliding filament theory*. The events of the sliding filament theory can be broken down into: (1) excitation, (2) coupling, (3) contraction, and (4) relaxation.
What is the mean arterial pressure?
The mean arterial pressure (MAP) is the average arterial pressure throughout the cardiac cycle and is calculated as diastolic pressure plus one third the pulse pressure. The normal values are usually between 90-100 mmHg. Mean arterial pressure is the mean driving pressure that tends to push blood from high pressure to low pressure through the circulation. It is imperative that an adequate driving pressure be maintained otherwise blood flow to the various parts of the body would be impaired. The mean arterial pressure can be calculated as follows: MAP = DBP + 1/3(PP)
What two factors contribute to the mean blood pressure?
The mean blood pressure is a function of two factors: *cardiac output* (Q) and *total peripheral resistance* (TPR). Cardiac output is equal to heart rate (beats per minute) times the stroke volume (in either mL/beat or L/beat). Because the resting stroke volume is around 70 mL/beat and the resting heart rate is around 72 beats per minute, the resting cardiac output is usually around 5 Liters per minute. Q = HR X SV
Why is blood pressure useful to measure?
The measurement of blood pressure provides valuable information regarding the pumping efficiency of the heart and the overall condition of the systemic blood vessels. It is generally stated that the systolic blood pressure indicates the force of contraction of the heart and that the diastolic blood pressure indicates the condition of the systemic blood vessels.
What is the most common mechanism that can lead to an action potential in a muscle cell?
The most common mechanism that can lead to the initiation of an action potential in a muscle fiber is the stimulation of a nerve (causing the release of acetylcholine into the neuromuscular junction). The *acetylcholine* released by the motor nerve combines with receptor sites located on the motor end-plate membrane. When acetylcholine binds to these receptor sites it causes the sodium and potassium permeability of this membrane to increase and leads to the depolarization of the membrane. In order for repolarization to occur, acetylcholine must be rapidly destroyed. The membrane contains an enzyme, *acetylcholinesterase*, which destroys acetylcholine. At the myoneural junction, the lifetime of an acetylcholine molecule is about 5 msec.
What is the mechanism of the sliding filament theory?
The myofilaments are the contractile elements of the muscle. The thick myofilaments are made up of myosin molecules. The globular end of the myosin molecule forms a *cross-bridge* ATP and therefore, acts as an enzyme (*myosin ATPase*) whose substrate is ATP. By itself, myosin has a low ATPase activity. However, when combined with actin, the activity increases. The energy released from splitting ATP produces a cross-bridge movement between the actin and myosin. The precise manner of this movement is still unknown but a suggested hypothesis for which considerable evidence exists involves a power stroke of the globular head of myosin which would pull the actin towards the center of the sarcomere. The myosin would then disengage and reattached to the next actin molecule and repeat the cycle. At the end of the cross-bridge movement, there is a dissociation of the myosin bridges from the actin. This is caused by the binding of a molecule of ATP to myosin. This reaction returns the bridge to its original state and makes it possible to repeat the cycle.
Why is ATP so important to the cross-bridge cycle?
The need for ATP in this series of events is exhibited at death. With death there is a loss of ATP and the muscles become stiff and rigid (known as *rigor mortis*) because the thin and thick filaments are cross-linked (bound together) and can't be pulled apart.
How is mean corpuscular hemoglobin concentration calculated?
The normal value range is 30-35 and the units can be considered as g of Hb per deciliter of red blood cells. It indicates the concentration of hemoglobin in an average red blood cell. MCHC (g/dL of cell) = (hemoglobin (g/dL of blood) X 100)/(hematocrit (% or mL of cells per dL of blood)
What are parasympathetic effects on the heart?
The parasympathetic nervous system innervates the heart via the *vagus nerve*. The vagus nerve endings that innervate the heart terminate in the vicinity of the SA node and the AV node. Parasympathetic effects are mediated by the release of *acetylcholine*. Acetylcholine binds with *muscarinic cholinergic* receptors at the SA node and causes a decrease in heart rate. The effects of acetylcholine on the heart can be blocked by the drug *atropine*, which binds the muscarinic receptors. Atropine has no direct action on the heart; it functions simply to prevent acetylcholine from binding the muscarinic receptors.
What is the ejection fraction?
The percentage of the blood in the heart that is ejected is called the *ejection fraction*; this value is normally above 55%. EF = SV/EDV
What is the latent period?
The period between stimulation and the buildup of tension.
What is the fifth Korotkoff sound?
The point at which the sound ceases completely is called the end diastolic pressure. It is sometimes recorded along with the systolic and diastolic pressures (e.g. 120/80/75).
What is the primary function of the heart?
The primary function of the heart is to pump blood to the body's tissues. To move blood efficiently the heart must: receive adequate amounts of blood through returning veins, ensure a unidirectional flow of blood through its chambers by means of valves, and effectively pump the blood out through the arteries. The period from the end of one heart contraction to the end of the next is called the *cardiac cycle*. This cycle involves a series of electrical and mechanical events taking place in the heart during one heartbeat.
What are the areas of cardiac auscultation?
The principal areas of cardiac auscultation (areas where the sounds are best heard) are located on the anterior chest wall. The *aortic area* is at the second right intercostal space. The *pulmonic area* is at the second left intercostal space. The *tricuspid area* is at the fourth intercostal space at the left sternal border. The *mitral area* is near the cardiac apex, which is approximately located at the fifth intercostal space at the mid-clavicular line (note that this is not the location of the mitral valve, but the blood that goes through the mitral valve is directed towards the apex of the heart).
How fast does the arterial pulse wave travel?
The rate at which this wave travels is much faster than that of the flowing blood. Velocity rates of the pulse wave varies from about 4 m/sec in the aorta and 8 m/sec in large arteries to 16 m/sec in small arteries of young adults. Thus the pulse is felt in the radial artery at the wrist about 0.1 sec after the peak of systolic ejection into the aorta. As the arteries become more rigid with advancing age, the pulse wave travels faster.
What is the second heart sound?
The second heart sound is produced near the beginning of ventricular diastole (end of ventricular systole) and thus is sometimes used to indicate the end of the ventricular ejection period. The second heart sound is caused mostly by the *closing of the semilunar valves* and the resulting vibrations in the ventricles and arteries (however, it can also be affected by the opening of the AV valves). The sound produced is a *higher pitch* than the first heart sound because of the higher pressure in the arteries. It is commonly called the "dub" sound of the heartbeat.
What is the second Korotkoff sound?
The sounds become a softer murmur during the next 10 to 15 mmHg of drop in pressure.
What is the third Korotkoff sound?
The sounds become louder again and have a sharp thudding quality during the next 1o to 15 mmHg of decreased pressure.
What is the relationship between cuff pressure and Korotkoff sounds?
The sounds heard over the artery during blood pressure determination by the auscultory method are known as *Korotkoff sounds*.
What is the fourth Korotkoff sound?
The sounds suddenly become muffled and reduced in intensity. The pressure at this point is termed the diastolic pressure. This muffled sound continues for another 5 mmHg decrease in pressure.
What is the dicrotic notch?
The strength of the pulse is determined by the pulse pressure. A small oscillation on the falling phase of the pulse wave, the dicrotic notch, is caused by vibrations set up when the aortic semilunar valve snaps shut. The blood in the aorta rebounds against the arterial walls and a slight increase in pressure is produced.
What is the third heart sound?
The third heart sound is caused by the *turbulence associated with the rapid filling of the ventricles shortly after the AV valves open*.
What are the three types of polycythemia?
There are three forms of polycythemia: 1) relative polycythemia, 2) polycythemia vera, and 3) secondary polycythemia.
What are the types of granulocytes?
There are three types of granulocytes: 1) *neutrophils*, 2) *eosinophils*, and 3) *basophils*. Their names are based on their affinity for different stains used in histology. Granulocytes range in size from 10-15 micrometers in diameter. The granules in neutrophils and eosinophils are lysosomes. However, the granules in the basophils contain heparin and histamine, which can be released into the circulation when necessary. Because the nuclei of granulocytes look irregular and lobular, they are also known as *polymorphonuclear* (many shaped) leukocytes. Neutrophils and to a lesser degree, eosinophils destroy invading pathogens by *phagocytosis*. Basophils release histamine, a substance that causes the vasodilation associated with the inflammation response.
How is the cross-bridge cycle regulated?
There are two "regulator" proteins which prevent spontaneous cross-bridge activity. *Troponin* and *tropomyosin* are found on the thin filaments and prevent (inhibit) actin from combining with myosin in the resting muscle by "covering" actin's myosin binding sites. Calcium ions are responsible for initiating and terminating the contractile activity. The calcium ion removes the inhibitory effect of troponin and tropomyosin by binding to the troponin molecule. This shifts the tropomyosin molecule to "uncover" the myosin binding site of the actin. Muscle contraction is initiated when calcium ions bind troponin and contractile activity stops when calcium ions are removed from the cytoplasm (and thus removed from troponin).
What are the types of agranulocytes?
There are two types of agranulocytes: 1) *lymphocytes* and 2) *monocytes*. Some agranulocytes are produced in lymphatic tissue (from cells originating in the bone marrow) while others are produced in the bone marrow. They are between 10 and 20 micrometers in diameter. Because of its relatively large nucleus, there is a reduced amount of the agranular, relatively homogeneous cytoplasm. Lymphocytes are smaller than monocytes and are easily identified by their round nuclei and scant cytoplasm. Monocytes have kidney-bean-shaped nuclei and their cytoplasm has a ground glass appearance.
What is chronotropy?
Things that influence heart rate are said to have a *chronotropic* effect. For example, acetylcholine has a *negative chronotropic* effect on the heart (decreases heart rate). Things that influence the strength of contraction are said to have an *inotropic* effect. For example, epinephrine and norepinephrine have a *positive inotropic* effect on the heart.
What is the PR interval?
This interval represents the time delay between the depolarization of the atria and the ventricles and is measured from the beginning of the P wave to the beginning of the QRS complex. This interval *normally lasts 0.12-0.20 seconds*. It is used to *evaluate the function of the AV node*. For example, if the PR interval is greater than 0.2 seconds every beat the subject has a *first degree AV block*, and represents a slowing of action potential propagation across the AV node.
What is the QRS interval?
This interval represents the time for the impulse to be distributed over the entire ventricular myocardium and is measured from the beginning of the Q wave to the end of the S wave. This interval usually lasts *between 0.08 and 0.12 seconds*.
What is the QT interval?
This interval represents the total time between ventricular depolarization and repolarization, and is measured from the beginning of the QRS complex to the end of the T wave. At a heart rate of 70 beats per minute it is usually about *0.35 seconds in duration*, but the duration of the QT interval is very heart rate-dependent. The lower the heart rate is, the longer the QT interval.
What is the conduction system of the heart?
This system consists of: 1) the *sinoatrial node* (SA node) in which the normal rhythmic self-excitatory impulse is generated; 2) the *atrioventricular* (AV node) in which the impulse is delayed before entering the ventricles; 3) the *atrioventricular bundle* which conducts impulses from the atria, through the fibrous skeleton, into the ventricles, and 4) atrioventricular *bundle branches* (right and left) which conduct the impulses to all parts of the ventricles through the *Purkinje fiber network*. The components of the conduction system are modified cardiac cells that are specialized in the generation and conduction of electrical impulses.
How do you approximate the mean electrical axis on an EKG?
a) To determine if the electrical activity of the heart is spreading to the left or the right, measure the upward (+) and downward (-) deflections of the QRS in limb lead I. If the value is more positive the electrical activity is moving more towards the positive electrode or left arm and they are in either the normal quadrant or in left axis deviation. If the value is more negative the electrical activity is moving more towards the right arm and they are in either right or extreme right axis deviation. b) To determine if the electrical activity is moving superiorly or inferiorly in the body, the same procedure is used in lead AVF. c) In most individuals, the QRS complex is mostly positive (upwards) in both limb leads one and in AVF, thus their mean electrical axis is in the normal quadrant.
What are erythrocytes?
*Erythrocytes* are biconcave disk-shaped cells containing the respiratory pigment *hemoglobin*, which allows the cell to bind oxygen and also gives the cell its red color. The erythrocyte is approximately 8.5 micrometers in diameter and about 2.4 micrometers in thickness at its edge. The biconcave shape of the cell increases the surface area for diffusion. This is extremely important because the primary function of the red blood cell is to transport oxygen and carbon dioxide. During its development in the bone marrow, the red blood cell loses its nucleus. Due to its biconcave shape, more light passes through the center of the cell than its periphery. This give the cell a donut-shaped appearance when examined under the light microscope. Abnormally shaped erythrocytes (e.g. sickle cells, microcytes) are frequently due to the presence of abnormal hemoglobin molecules or to an abnormal amount of hemoglobin. Bending and twisting as they pass through the circulatory system, the pliable red blood cells have an average circulation life of 125 days. Complete replacement of red blood cells occurs once every four months. The bone marrow produces hundreds of billions of red blood cells daily to replace those destroyed. The average number of red blood cells is approximately 5,000,000 cells per cubic millimeter of blood. Functionally, the red blood cells participate in: 1) the transport and release of oxygen and carbon dioxide, 2) the buffer system of the blood, and 3) the coagulation of blood (minor role).
What is ischemia?
*Ischemia* is a term that means that a tissue's oxygen demand is greater than the oxygen supplied to it. If the heart is experiencing such a supply/demand mismatch, we would call it *myocardial ischemia*. If the myocardium is deprived of oxygen for too long, then the cells will eventually being to die (*myocardial infarction*). It is worth noting that ischemia is reversible if either there is an increase in oxygen supply or a decrease in oxygen demand. However, once the cells begin to die, the damage is done and this is, for the most part considered irreversible (although there have been some promising research findings suggesting that some of the dead cells can be replaced, though not revived). Because the *myocardial oxygen demand*, the amount of oxygen that the heart requires, is of such importance, it is useful to have a simple way of estimating it.
What is leukocytosis?
*Leukocytosis* is a condition where the number of leukocytes exceeds the upper limit of the normal range. A count above 50,000 per cubic millimeter indicates a possible malignant proliferation of white blood cells known as *leukemia*. Any count above 100,000 per cubic millimeter is almost certain to be caused by leukemia. An increased leukocyte production in most cases is a favorable indicator of the body's response to the invasion of foreign material such as parasites, bacteria, and toxins.
What is myoglobin and why is it important?
*Myoglobin* is a protein similar to hemoglobin that plays a role in storing oxygen and in transferring oxygen within the muscle cells. The presence of myoglobin causes the more aerobic fibers (I and IIA) to appear slightly red in appearance and the less aerobic fibers to appear white.
What is polycythemia vera?
*Polycythemia vera* (true polycythemia) is an increase in both the concentration of red blood cells and total red cell mass due to an increased production by the bone marrow. The cause in most cases is unknown but it can be symptomatic of certain malignancies of the brain, bone marrow, and kidney.
What is relative polycythemia?
*Relative polycythemia* is a relative increase in the number of red blood cells as a result of the loss of the fluid portion of the blood. It may occur in the case of dehydration, severe burns and shock.
What is secondary polycythemia?
*Secondary polycythemia* is a condition occurring as a physiological response to chronic arterial hypoxia. The hypoxia may be associated with living at high altitude environments or may occur in other low blood oxygen states. A deficiency or qualitative defects in platelets can cause problems in blood coagulation. The defects may be acquired or hereditary.
What is ventricular ejection?
*Ventricular ejection* begins when the aortic and pulmonary valves open. Rapid at first, ejection of blood slows down as systole progresses. Ventricular pressure rises to a maximum and then slightly decreases before ventricular systole ends. Peak pressure for the left ventricle is around 120 mmHg, while that for the right ventricle is 25 mmHg or below. Late in systole, the aortic pressure is actually higher than the pressure in the left ventricle, but for a short time, momentum keeps the blood moving away from the heart. The falling ventricular pressure drops more rapidly once contraction is completed. This period of about 0.04 seconds is known as *protodiastole*. This lasts until the momentum of the ejected blood is overcome and the aortic and pulmonary valves snap closed, setting up transient vibrations in the blood and blood vessel walls.
What are the steps in excitation, coupling and contraction?
1) Acetylcholine release from motor neuron. 2) Binding of acetylcholine to acetylcholine receptors, allowing a lot of sodium to diffuse into the cell and some potassium to diffuse out of the cell, resulting in the formation of an end plate potential. The end plate potential in the end plate region of the sarcolemma results in the formation of an action potential in surrounding regions of the sarcolemma. 3) Action potential initiated and spreads over the sarcolemma. 4) Inward spread of depolarization along T tubules. 5) Release of calcium ions from lateral sacs of sarcoplasmic reticulum and into the sarcoplasm. 6) Binding of calcium ions to troponin, uncovering myosin binding sites on actin. 7) Formation of cross-bridges between actin and myosin. 8) Myosin cross-bridges bend and produce a power stroke. The thin filaments slide over thick filaments resulting in shortening of the sarcomere. If calcium is still present, the active sites on the actin filaments will remain exposed and steps 7 and 8 will go through another cycle.
What are the 3 anatomical and physiological properties of the heart?
1) Automaticity 2) Functional Syncytium 3) Conduction System
What are the steps in relaxation following an action potential?
1) Calcium ions are actively pumped back into the sarcoplasmic reticulum. 2) Release of calcium ions from troponin. 3) Tropomyosin snaps back into place and inhibits interaction between actin and myosin.
What is the function and WBC percentage of eosinophils?
2-4% of total WBCs Detoxification of foreign proteins & other substances
What is the function and WBC percentage of lymphocytes?
28% Antibody production (B lymphocyte); cellular immune response (T-lymphocyte)
What is the function and WBC percentage of neutrophils?
65% of total WBCs Immune defense (phagocytosis)
What is the isoelectric line?
The isoelectric line is the plat parts of the EKG, for example, between the T and P waves or between the P wave and the QRS complex.
What is blood coagulation?
After the formation of the platelet plug, the process of forming a blood clot (coagulation) begins. Coagulation is a detailed series of chemical events that can be divided into three stages or phases. Stage I involves the sequence of chemical events that lead to the production of the enzyme prothrombin-converting factor also known as *prothrombin activator*. During stage II, prothrombin activator convers *prothrombin* to *thrombin*. In stage III thrombin converts *fibrinogen* to *fibrin* by proteolytic action. The long fibrin molecules form an insoluble network that acts to seal the site of blood vessel damage. Two pathways, *intrinsic* and *extrinsic*, may lead to the formation of the fibrin clot. the chain of chemical events has been called a "cascade" o "waterfall" sequence of events. There are 13 clotting factors, along with blood platelets, that make coagulation possible. Calcium and phospholipids are essential cofactors in certain steps of the pathways. The calcium ions are furnished by the plasma, while the phospholipids are provided by the participating platelets. After the blood vessel has repaired itself by producing new endothelial cells and connective tissue, the clot is no longer needed. The clots are dissolved by the enzyme *plasmin*. The conversion of plasminogen, an inactive blood protein, to plasmin is triggered by the Hageman factor (factor ZII). This fibrinolytic system is much slower than the clotting system, so that adequate amounts of plasmin are achieved only after the clot has completely formed.
What is normal sinus rhythm on an EKG?
All intervals are in the normal range; regular rhythm at a pace of 60-100 beats per minute; each QRS is preceded by normal P wave; PR interval contstant.
What is an EKG?
An *electrocardiogram* (EKG) is a graphic depiction of the electrical activity of the heart. The EKG demonstrates a very organized and reproducible sequence of electrical events that occur within the heart. Examination of this sequence of electrical events can be useful to determine if the mechanical events (pumping of blood) of the heart are also occurring in the proper manner. Abnormal electrical events in the EKG may result in abnormal mechanical events which could compromise cardiac output and normal delivery of oxygen. When examining an EKG it is important to remember that the sequence of events represents a very complex compound depiction of the electrical events in the heart. Every cell in the myocardium is depolarizing and then repolarizing. In order to produce a productive contraction, some of the myocardial cells need to be stimulated sooner than others. The heart has three important anatomical and physiological properties that can account for this very reproducible event.
What is an extra systole?
An *extra systole* is essential a premature beat. If an extra systole is initiated in the ventricles, then it is called a *premature ventricular contraction* (PVC). PVCs are frequently followed by compensatory pauses. A *compensatory pause* is a period of time after a premature beat when there is no activity. These pauses are a result of the normal automaticity of the heart. The SA node fired during the premature beat, but was unable to stimulate a contraction because it was already contracting. The SA node maintains its normal firing pattern and will pick up right where it is supposed to. Since the previous beat was premature, the amoutnm of time between it and the next beat will be a bit longer.
How does a change in the number of extracellular potassium ions affect heart rate and contractility?
An increase in the concentration of extracellular potassium ions (K+) can decrease the resting membrane potential. Remember, the resting membrane potential is partially dependent on the maintenance of a higher K+ concentration on the inside of the cell than in the extracellular fluid (ECF). An increase in blood potassium is called *hyperkalemia*. An increase in ECF K+ can cause a decrease in heart rate and can cause a mild to severe decrease in contractility. Severe hyperkalemia can slowly result in atrial paralysis, slow ventricular conduction, and possibly ventricular arrhythmias. In extreme hyperkalemia the conduction rate may be so depressed that ectopic pacemakers develop in the ventricles and lead to fibrillation. *Hypokalemia*, on the other hand, can slow the conduction in the AV node; possibly even causing AV blocks.
How does an increase in the number of extracellular calcium ions affect heart rate and contractility?
An increase in the extracellular concentration of calcium above normal affects both the electrical properties and the contractility of muscle. In fact, many of the drugs, neurotransmitters, and hormones that influence cardiac contractility do so by affecting the amount of calcium in the cytoplasm of cardiac cells during contraction. *Hypercalcemia*, an increase in extracellular calcium, increases contractility and may or may not cause a decrease in heart rate. Hypercalcemia also can cause a number of arrhythmias, especially ventricular ectopic foci (PVCs) and can also cause an increase in blood pressure.
What is thrombocytosis?
An increase in the number of circulating platelets is known as *thrombocytosis* or *thrombocythemia*. It may occur pathologically as the result of a malignancy or with polycythemia vera. Under normal conditions, it may occur during menstruation, pregnancy, or severe exercise.
What are muscle fibers?
An individual skeletal muscle such as the biceps brachii is comprised of many muscle cells known as *muscle fibers* or *myofibers*. The muscle fibers are elongated, multinucleated and have striations at regular intervals. The fibers run parallel to one another. Skeletal muscle is often referred to as "striated" muscle because of its appearance.
What is the arterial pulse wave?
As blood in the heart's left ventricle is forced into the aorta during systole, not only does the blood advance in the vessels but a pressure wave travels along the arteries. An expansion of the arterial walls occurs and is palpable as the pulse. During the cardiac cycle, one sees within the arteries a varying of blood pressure. The pressure changes range from the highest pressure, systolic, due to ventricular contraction, to the lowest pressure, diastolic, when the ventricles are relaxed and there is no blood flowing through the semilunar valves. The recording of arterial pressure changes during one cardiac cycle is called an arterial pulse wave. The shape and magnitude of the arterial pulse wave are directly related to the stroke volume and inversely related to the elasticity of the arterial walls. As the arteries lose their elasticity, stroke volume decreases and the pulse pressure increases.
What is stroke volume?
At rest, the volume of blood ejected by each ventricle is about 70-90 mL, this is the resting *stroke volume*. Stroke volume is equal to *end diastolic volume* (EDV, the volume of blood in the ventricle at the end of diastole) minus the *end systolic volume* (ESV, the volume of blood remaining in the ventricle at the end of systole). SV = EDV - ESV
What is a pulse pressure?
At the beginning of left ventricular contraction, the ejected blood flows faster going into the aorta than it does leaving the arterioles. As a result, the ejection of blood by the ventricle faces opposition of the blood remaining in the aorta from the previous ventricular ejection. The tension in the aortic wall increases as the vessel distends to accommodate more blood and arterial pressure increases. After the aortic valve closes the elastic elements of the aorta cause the walls of the aorta to recoil, resulting in a secondary increase in aortic and arterial pressure. This secondary rise in pressure as a result of the aortic wall recoil is transmitted down the arterial tree. A pulse of pressure is thus created, moving rapidly down the aorta and conducted along the arterial system. The velocity at which this pulse is transmitted is dependent upon the elasticity of the vascular walls and on the blood pressure.
What happens during ventricular systole?
At the beginning of ventricular systole, the tricuspid and mitral valves close. There is an initial period of *isovolumetric ventricular contraction* where the ventricular muscle shortens relatively little but the pressure inside the ventricles rises sharply as the ventricular myocardium presses on the blood. About 0.05 seconds later, the *pulmonary* and *aortic valves* open as pressures in the right and left ventricle exceed the pressures in the pulmonary artery and aorta. The AV valves bulge into the atria during the isovolumetric contraction. This creates a small but sharp rise in atrial pressure.
What is the role of calcium in the cross-bridge cycle?
Calcium ions are stored in the *lateral sacs* of the *sarcoplasmic reticulum*, so that there is a high concentration of calcium ions in the SR and a low concentration of calcium ions in the cytoplasm surrounding the myofilaments. When an action potential is generated and is conducted down the membrane of a muscle cell, it spreads to the interior of the cell's vast sarcoplasmic reticulum network via the *transverse tubules*. Depolarization of the SR causes the rapid release of calcium ions and allows calcium ions to surround the myofilaments and bind to troponin. Contraction takes place as long as calcium ions are exposed to the myofilaments. After cessation of the action potential, relaxation occurs as calcium ions are actively pumped back into the SR via the SR's *calcium ion pumps (or calcium ion ATPases, also called SERCAs)*, thus removing the calcium ions from cytoplasm bathing the myofilaments. Calcium is released from the SR via specialized *calcium release channels*, which are called *ryanodine receptors*. About half of these RYRs are associated with specialized receptors in the T-tubule membrane, which are called *dihydropyridine receptors*. DHPRs are sensitive to changes in voltage (changes in membrane potential). Thus, when an action potential spreads down the T-tubule, the DHPRs are activated and cause the ryanodine receptors to open, which allows calcium to diffuse out of the SR and into the sarcoplasm.
What are the aerobic/oxygen demands of the heart?
Cardiac muscle cells have a very poor ability to use glycolysis; the myocardium is thus very dependent upon aerobic metabolism to meet the cardiac muscle's ATP demands. It is essential, then, that the myocardium continuously receive adequate quantities of oxygen, which, in turn, are dependent upon adequate blood flow in the *coronary arteries*, the blood vessels that supply the heart with oxygenated blood
How does the heart set its own pace?
Each portion of the conduction system exhibits the property of automaticity. The SA node usually spontaneously depolarizes at a rate of about 70 times per minute. Each segment of the conduction system spontaneously depolarizes at a progressively slower rate. If the SA node stopped having action potentials, or if each part of the heart was dissected and studied separately, the atrial muscle cells would depolarize approximately 60 times per minute. In the absence of the SA node, or atrial muscle initiation of depolarization in the heart, the AV node could take over as the pacemaker. The AV node depolarizes at an inherent rate of approximately 50 times per minute. The Purkinje fibers could take over as the pacemaker for the ventricles if the SA node and AV node failed. The Purkinje fibers depolarize at an inherent rate of about 30 times per minute. The inherent rate of depolarization in the ventricles is about 25 times per minute. Due to the arrangement of the myocardial cell in a functional syncytium the cell that reaches threshold first will control the rest. Thus, since the SA node normally depolarizes first, it usually serves as the pacemaker of the heart, depolarizing around 70 times per minute in an average individual.
What is the functional syncytium of the heart?
Each region of the heart has its own intrinsic rate of sodium leaking and therefore of beating. For example, SA node = 70 beats/min, Atrium = 60 beats/min, AV node = 50 beats/min, Purkinje fibers = 30 beats/min, and ventricle = 25 beats/min. The heart is also a *functional syncytium*. This means that all of the myocardial cells function as one. This characteristic is the result of the *gap junctions* that are located in the *intercalated discs* between the myocardial cells. Therefore the first cell to reach threshold will start all of the remaining cells. However, an action potential can only move from the atria to the ventricles through the common AV bundle due to the lack of the gap junctions in the fibrous skeleton. The SA node is normally the pacemaker. If for some reason the SA node is not working correctly, the next slower region will become the pacemaker.
What is hypertension?
Hypertension is a sustained elevation of the systemic arterial pressure. Currently, hypertension is diagnosed if the SBP is greater than 140 and/or the diastolic is greater than 90 mmHg. Since arterial pressure is determined by the cardiac output and the peripheral resistance, hypertension can be produced by elevating the cardiac output or increasing the peripheral resistance. Sustained hypertension is usually due to increased peripheral resistance. The hypertension that follows constriction of the renal blood supply or compression of the kidney is called *renal hypertension*. Hypertension is a very commony abnormality in humans. It can be produced by many disease (i.e. adrenocortical diseases, tumors of adrenal medulla, tumor of juxtaglomerular cells, narrowing of renal arteries, renal disease, narrowing of the aorta, and severe polycythemia). However, most cases of hypertension are classified as *essential hypertension* which means we don't know why they occur. A number of serious disorders may be caused by hypertension. These include cardiac muscle hypertrophy, arteriosclerosis, myocardial infarction, thromboses of cerebral vessels, cerebral hemorrhage, an renal failure.
How are the filaments arranged in a 3D structure?
If a cross section of the myofibril is taken, one can look at the arrangement of actin filaments and myosin filaments in a different plane. If the cross section is taken in the region of the I-band, one sees a regular hexagonal arrangement of the actin filaments. In the area of overlap between actin and myosin, the arrangement is a central myosin filament surrounded by six hexagonally arranged actin filaments. Comprising the central H zone of the A band are only myosin filaments, which in cross section will appear as a larger hexagonal pattern.
What is sinus bradycardia?
If a subject's heart rate is below 60 beats per minute they are said to be in *sinus bradycardia*.
What is sinus tachycardia?
If a subject's heart rate is over 100 beats per minute they are said to be in *sinus tachycardia*.
What is normal sinus rhythm?
If all intervals are normal and all waves are present and if the subject's heart rate is between 60 and 100 beats per minute, then they are in *normal sinus rhythm*.
What is hemophilia?
If any of the clotting factors, cofactors, or platelets are missing or deficient, the clotting mechanism is impaired, resulting in hemophilia. Several inherited diseases of blood clotting involve defective genes for clotting factors. The most common genetic defect, hemophilia A, is caused by a defective factor VIII. Many clinical tests have been developed to assess hemostasis and its disorders.
Do skeletal muscle fibers work on an all-or-none basis?
If given an adequate stimulus (threshold stimulus or greater), a muscle fiber will contract maximally. Thus, skeletal muscle fibers are said to work on an *all or none* basis. Motor units also work on an all or none basis. However, for a whole muscle, the degree of contraction can be modified by changing the number of muscle fibers that are activated. A relatively weak stimulus will cause only a few motor units to be stimulated and will produce a small degree of contraction. As the stimulus is increased, more and more motor units become stimulated and the degree of contraction will increase. Finally, when a stimulus is high enough to stimulate all the muscle fibers of the whole muscle, all the fibers will contract, causing the whole muscle to contract maximally (*maximal contraction*). Action potentials in neurons, muscle fibers, motor units. DOES NOT apply to a whole muscle.
What is the U wave?
If present, the U wave represents repolarization of Purkinje fibers and/or the ventricular septum.
What are premature contractions?
If some other cell in the heart should depolarize before the SA node it would become the pacemaker, at least for that beat of the heart. For example, if a myocardial cell in the atria should happen to depolarize before the SA node, it would result in a premature beat. If the premature beat is initiated in the atria, they are referred to as *premature atrial contractions* (PAC). If a premature beat is initiated in the ventricles they are referred to as *premature ventricular contractions* (PVC). These (atrial or ventricular myocardial) cells that initiate a heart beat, but that are not normally the pacemaker are referred to as *ectopic foci*. These PAC's and PVC's alter the normal cardiac cycle and therefore result in an abnormal electrical rhythm. An abnormal heart rhythm is referred to as an *arrhythmia*. The normal electrical rhythm of the heart is referred to as *normal sinus rhythm*.
What are murmurs?
If the heart valves are damaged, they produce abnormal heart sounds called *murmurs*. Murmurs may be associated with *insufficient valves* (which allows backward flow through the valve) or with narrowing of a valve's opening (*stenosis*). If the murmur is heard during ventricular systole, is is called a *systolic murmur*, and if it is heard during ventricular diastole, it is called a *diastolic murmur*. Aortic stenosis and AV valve insufficiency are causes for systolic murmurs, while incomplete closure of the semilunar valves may bring about a diastolic murmur. Septal defects and vascular abnormalities may also produce murmurs. Some murmurs are of the not pathological variety and may be due to turbulence in blood flow. One of the most common (especially in women and athletes) types of valve problems is *mitral valve prolapse* (MVP). Mitral valve proplapse means that when the pressure in the ventricle exceeds the pressure in the atria and the mitral valve closes, it "lapses" slightly backwards into the atria. In some, but not all, cases of MVP there is some regurgitation of blood from the ventricle into the atria.
How are cardiac action potentials unique?
In addition to the myocardial properties listed above it is also important to understand that cardiac muscle cells (myocardial cells) do not produce a "typical" action potential. This is due to the presence of *slow calcium channels* in the myocardium. These channels are opened at the point of stimulus like the sodium channels; however, they open much slower and remain open much longer. This produces a *plateau phase* in the action potential immediately following depolarization. As the slow calcium channels close the potassium channels open and the cell repolarizes. The end result is an action potential that usually is 0.25 to 0.3 seconds in duration, much slower than typical skeletal muscle. This long action potential results in an extended *refractory period*. This accounts for the inability of the heart to be tetanized.
How much time is spent in systole and diastole in humans?
In humans, 60% of the time is spent in ventricular diastole, while 40% is spent in ventricular systole. See handout
What is mean corpuscular hemoglobin concentration?
In order for red blood cells to function properly they should also have the correct amount of hemoglobin. One can calculate the mean corpuscular hemoglobin concentration to obtain a rough estimate of how much hemoglobin there is relative to red blood cells. Normal values for MCHC are between 30-35 grams per deciliter of cells.
What is cardiovascular regulation?
In order to maintain homeostasis, the body must maintain an adequate driving pressure (arterial pressure) to pump freshly oxygenated blood (as well as other nutrients, hormones, etc.) to the body's tissues and to remove metabolic byproducts such as carbon dioxide. If arterial pressure drops too low it will not be possible to move blood against the forces of gravity up to the brain or to perfuse the body's tissues. The brain cannot function without oxygen because it cannot create ATP anaerobically. A number of complications can also arise from having chronically elevated blood pressure. In order to survive, blood pressure must be maintained within an appropriate range (homeostasis). *In general, the body response to changes in pressure by changing cardiac output and/or by changing blood vessel radius). Thus, if blood pressure gets too low, the body can respond with an increase in cardiac output and/or by constricting the blood vessel (decreasing the radius).
How are blood pressure and blood flow pusatile in nature?
In the aorta and other large arteries both blood pressure and blood flow are pulsatile in nature. During systole of the left ventricle, arterial pressure increases and during ventricular diastole, it decreases.
What can looking at the mean electrical axis of the heart tell us?
Looking at the mean electrical axis of an individual's heart can give us valuable information about possible *hypertrophy* and/or *infarction* of part of the myocardium. If the myocardium is hypertrophied, the increase in the size of the myocardium in the hypertrophied area causes a relative increase in the electrical activity of that area. This means that the mean electrical axis will tend to shift towards hypertrophy due to this increase in electrical activity. On the other hand, if the myocardium is *necrotic* (dead) in a particular area, because these cells are no longer living they do not depolarize when an action potential reaches them. The result of this lack of electrical activity is that the mean electrical axis will tend to shift away from infarction (e.g. a left ventricular myocardial infarction would be expected to cause a right shift in the mean electrical axis).
What are normal values for hemoglobin concentrations in adults?
Males: 15.4 g/dL Average (13.5-17.5 g/dL range) Females: 13.3 g/dL Average (11.5-15.5 g/dL range)
What is a twitch?
Mechanical response of muscle to a single action potential.
What do monocytes and lymphocytes become?
Monocytes undergo a change when they enter connective tissues and become phagocytic cells called *tissue macrophages*, which act to remove foreign particles or damaged tissue. Neutrophils also play a phagocytic role in infected or inflamed tissues. Lymphocytes are involved in specific immune responses. Lymphocytes are first produced in the embryonic bone marrow, which then seeds the other lymphocyte-forming sites (i.e. *thymus, lymph nodes, and spleen*). The thymus then sends cell to other body sites and apparently regulates the general rate of lymphocyte production at all these locations through the release of a hormone. All lymphocytes may be categorized in terms of their development and maturation, those developing in the thymus gland (*T-lymphocytes*) and those lacking thymus influence (*B-lymphocytes*). T-lymphocytes function in the *cell-mediated* immune response and B-lymphocytes function in the *antibody mediated* immune response
How do muscle fibers produce different amounts of control?
Movements of the body involve smooth, coordinated control. Muscular activity for any movement requires that the muscle be able to change the strength of contraction or the extent of shortening in proportion to the load placed on it. The degree to which a skeletal muscle contracts is dependent upon the number of motor units activated within the muscle. The number of muscle fibers in a motor unit varies. In extraocular and hand muscles where fine, graded, precise movement is necessary, there are 3-6 muscle fibers per motor unit. In a large muscle where degree of control is not as important, there may be as many as several hundred fibers per motor unit.
What is isotonic contraction?
Muscle changes length resulting in movement. a) Concentric: muscle tension exceeds load resulting in muscle shortening. b) Eccentric: load exceeds muscle tension resulting in muscle lengthening.
What is isometric contraction?
Muscle contracts increasing tension but no shortening occurs.
What is the length-tension curve of a muscle?
Muscle is an elastic tissue which exhibits the ability to be stretched. However, the degree of stretch on a muscle will affect its ability to produce force. Muscle tension during a stretch can be divided into three types of tension: passive, active, and total. *Passive tension* is the tension in the muscle due to its elastic characteristics. For example each of the connective tissues associated with skeletal muscle (tendons, epimysium, perimysium, and endomysium possess some amount of the protein *elastin*. Unlike the other principal protein in these connective tissues, *collagen*, elastin is very elastic). Additionally, many components within the fibers contribute to the elastic nature of muscle (and thus to the passive tension). For example, the protein *titin*, also contributes significantly to the passive tension. *Active tension* is the force produced by contractile activity and *total tension* is equal to the active plus the passive tension.
What is tetanus?
Muscle response where repetitive stimulation at a sufficiently rapid frequency produces a sustained maximal contraction.
How is blood pressure measured?
One indirect method of estimating systemic arterial blood pressure utilizes a stethoscope and a *sphygmomanometer* (blood pressure cuff). The sphygmomanometer is an inflatable rubber cuff with a pressure gauge attached to it. It is attached around a limb (usually arm) and as it is inflated, it collapses the artery underneath. A stethoscope bell is placed over the artery distal to the cuff. When the pressure of the cuff exceeds the pressure in the artery, the artery is collapsed and blood flow through it ceases. As pressure in the cuff is reduced, blood flow through the artery begins at a cuff pressure just below systemic arterial pressure. At this time, a sharp, tapping sound may be heard with the stethoscope over the artery. At this sound, cuff pressure is taken as an approximation of systolic pressure. In addition, as blood rushes into the arteries distal to the cuff, palpable pulses are produced at the wrist. Without a stethoscope, one can use this onset of pulse to determine systolic pressure. As pressure in the cuff is further reduced, the sounds made are most intense and then become suddenly muffled. This occurs at the level of diastolic pressure, where the artery remains open throughout the entire pulse cycle. Cuff pressure at the point of sound muffling is used as an approximation of diastolic pressure. As cuff pressure continues to be reduced, the sounds disappear completely and normal flow through the vessel is reestablished. Since the disappearance of the sound is easier to establish than muffling, and since there is only a few millimeters of mercury pressure change between the two, the disappearance of sound is commonly used in determining diastolic pressure.
What is the baroreceptor feedback mechanism?
One of the neural pressure control mechanisms, the *baroreceptor feedback mechanism* involves pressure receptors called *baroreceptors* in the internal carotid arteries and aorta. Information from these receptors is integrated by the *vasomotor center of the medulla oblongata*. When body position changes (i.e. supine to sitting to standing), the baroreceptors respond in an attempt to maintain a relatively constant arterial pressure. As the body assumes a more vertical position, gravity pools blood in thee extremities and there is a decrease in blood pressure in the carotid baroreceptor area. This elicits a baroreceptor reflex as neural activity leaving the baroreceptors decreases. This information is sent to the vasomotor centers with a resulting increase in sympathetic activity. This increased sympathetic activity produces vasoconstriction and an increased heart rate, thereby producing an increase in blood pressure. This minimizes the decrease in arterial pressure in the head and upper body. When there is an increased stimulation of the baroreceptors caused by an increased arterial pressure in the baroreceptor area, it results in an inhibition of vasoconstriction by the vasomotor center and a decreased heart rate.
How else can the mean electrical axis be shifted?
Other situations and conditions can alter the mean electrical axis. The mean electrical axis of individuals who are severely obese or pregnancy may be shifted to the left. The reason for this is that the fatty deposits or the fetus are pushing up on the diaphragm, which is in turn pushing the apex of the heart towards the left. It is also not uncommon in tall thin individuals to see a difference in mean electrical axis between the supine and standing positions. The cause of this difference is that when the individual is lying down many of the abdominal contents push up on the diaphragm, and thus on the heart. When they stand up the heart shifts back.
How do the heart valves close?
The action of the heart valves is passive. The valves don't move themselves, but are acted upon by pressure differences between the regions they separate. When the pressure in the atria is greater than the pressure in the ventricles, the AV valves are open, and blood flows from the atria into the ventricles (period of *ventricular filling*). When the pressure in the ventricles exceeds the pressure in the atria, the AV valves close, preventing backwards flow of blood from the ventricles into the atria (period of *isovolumetric ventricular contraction*). Eventually the pressure in the ventricles exceeds the pressure in the arterial trunks (the aorta and the pulmonary artery) the semilunar valves open, and blood is ejected from the heart into the systemic and pulmonary circulation (period of *ventricular ejection*). The semilunar valves close again when the pressure in the ventricles falls below the pressure in the arterial trunks (period of *isovolumetric ventricular relaxation*). Eventually the pressure in the ventricles again falls below the pressure in the atria and the ventricles begin to fill again (back to the beginning of the period of isovolumetric ventricular contraction). These cyclic changes in pressure and volume of the chambers are regulated by the electrical events in the cardiac cycle, and are responsible for the pumping actions of the heart.
What is contraction?
The active process of generating force; force exerted parallel to muscle fibers.
What is summation?
The adding together of individual muscle twitches to make strong concerted muscle movements; occurs by: a) increasing the number of motor untis contracting simultaneously (multiple motor unit summation)
What is formation of a platelet plug?
The adhesion and aggregation of platelets at the damaged area is an initial but temporary sealing phase (formation of a platelet plug). A change in the behavior of platelets is triggered by exposure to an abnormal (torn or rough) surface. The transformed platelets are called sticky platelets due to their adherence to the exposed surface and to one another. It has been found that undamaged vessels carry a net positive charge on their surface while damaged cells and the structure protein collagen have a net negative charge that enables the platelets with a net positive charge to bind on contact. The release of large amounts of ADP by the platelets as they degranulate (disappearance of cytoplasmic granules causes release of substances contained in the granules) increase the adhesiveness of the platelets. The ADP also causes additional platelets to become "activated" and adhere to the originally activated platelets. This sticking together by the platelets develops into a platelet plug.
What is the pulse pressure?
The amount of pressure built up during a pulse is called the pulse pressure. The pulse pressure is defined as the difference between the systolic and diastolic pressures. It is normally between 40 and 50 mmHg. PP= SBP - DBP
What is hemostasis?
The arrest of bleeding is known as *hemostasis*. When a blood vessel ruptures or is injured, the amount of blood lost is reduced by 1) *vascular spasm*, 2) formation of a *platelet plug*, and finally 3) blood *coagulation*.
How is arterial oxygen content calculated?
The arterial oxygen content is partly determined by the oxygen carrying capacity and partly by the arterial percent saturation of hemoglobin with oxygen; it represents the actual amount of oxygen carried per 100 mL of blood in the arterial circulation. Arterial oxygen content = Oxygen carrying capacity X SaO2
What is automaticity?
The cell membranes of most of the myocardial cells, especially *pacemaker cells* (e.g. SA and AV nodes), have an increased permeability to sodium. These "leaky membranes" allow sodium ions to gradually leak into the interior of the myocardial cell, resulting in a slow depolarization of the membrane. Because of the presence of voltage gated calcium channels, if the membrane depolarizes enough, the calcium channels open and allow an influx of calcium, causing further depolarization. Thus, as sodium and then calcium ions leak in, the membrane depolarizes and eventually reaches threshold. Once the cell reaches threshold an action potential will occur, and will ultimately result in depolarization and contraction of cardiac muscle cells. Therefore the heart has the ability to stimulate itself without any outside influence (i.e. it automatically depolarizes itself). Thus, unlike skeletal muscle, no neural input is required to initiate cardiac muscle contractions. The heart is innervated by both branches of the autonomic nervous system. However, these serve to increase the rate of depolarization (*sympathetic nervous system*) or decrease the rate of depolarization (*parasympathetic nervous system*), resulting in an increase or decrease in *heart rate*.
How are cell muscle membranes "excitable"?
The cell membranes of muscle are "excitable" membranes meaning they are capable of generating and propagating an action potential via mechanisms similar to that of nerve cells. Action potentials provide the signal for the initiation of contractile activity. This electrical signal in the membrane triggers off the chemical events of contraction and consequently, the process is known as *excitation-contraction coupling*.
What is the central nervous system ischemic mechanism?
The central nervous system ischemic mechanism is principally an emergency arterial pressure control system. It acts rapidly and extremely powerfully to prevent further decreases in arterial pressure if blood flow to the brain decreases to nearly lethal levels. It is sometimes referred to as the "last ditch stand" pressure control mechanisms.
What is the chemoreceptor mechanism?
The chemoreceptor mechanism involves chemo-sensitive receptors located in the two carotid bodies and several aortic bodies that are stimulated by decreases in oxygen or increases in hydrogen ions and carbon dioxide in the arterial blood. These receptors excite the vasomotor center to produce an elevation of arterial pressure.
What are systole and diastole?
The contraction of cardiac muscles is known as *systole* and the relaxation of cardiac muscle is known as *diastole*. The sequence of cardiac muscle contraction and relaxation during one cardiac cycle is: the atria are in systole while the ventricles are in diastole, followed by atrial diastole and ventricular systole. Thus, when the atria are contracting the ventricles are relaxed. The pressure in the atria is higher than in the ventricles and as blood pushes on the atrial side of the AV valve the valve cusps are pushed into the ventricle to an open position. Blood moves into the ventricles. During ventricular systole the pressure in the ventricles goes up while the pressure goes down in the relaxing atria. As blood tries to go from the ventricles back into the atria it catches in the valve cusps and pushes them into a closed position and prevents the blood from reentering the atria. When pressure in the ventricles exceed arterial pressure the semilunar valves are pushed into an open position and blood is ejected from the ventricles into the arteries. However, as the ventricles relax, ventricular pressure goes down (below arterial) and blood tries to reenter the ventricles. The blood fills the valve cusps and the valve orifice is closed.
How is the electrical activity of the heart recorded?
The electrical activity of the heart is recorded from the body by surface *electrodes*. The combination of two or more electrodes is used to evaluate the timing and the direction of the electrical activity. Each combination of electrodes is called an EKG *lead*. In each of the *limb leads* one electrode is designated as positive (+) and one is designated as negative (-). In each of the *augmented voltage leads* one electrode is designated as positive (+) and two electrodes are designated as negative (-). The *precordial leads* (also called *chest leads*) are unipolar; they only have a single electrode, which is a positive (+) electrode. If the wave of depolarization (the spread of electrical activity) is moving towards the positive (+) electrode, it results in an upward deflection of the recording. A wave of depolarization moving away from the (+) electrode causes a downward deflection in the recording. The opposite is true for a wave of repolarization.
At which auscultation areas will the heart sounds seem loudest?
The first heart sound (closing of the AV valves) should seem louder at the AV valve areas and the second heart sound (closing of the semilunar valves) should seem louder at the semilunar areas.
What is the first heart sound?
The first heart sound is produced at the beginning of systole and is caused by the *closure of the atrioventricular (AV) valves* and the opening of the semilunar (SL) valves (mostly AV closure). This sound has a *low pitched tone*, commonly called the "lub" sound of the heartbeat.
What is tension?
The force exerted.
What are the formed elements?
The formed elements in blood include *thrombocytes* (platelets), *erythrocytes* (red blood cells) and *leukocytes* (white blood cells). It should be noted that, while there are several types of formed elements, all of the formed elements originally started out as the same type of cell in the bone marrow; as an *undifferentiated pluripotent stem cell (UPSC)*.
What is the fourth heart sound?
The fourth heart sound is caused by the *turbulence associated with the passage of blood from the atria into the ventricles during atrial contraction* (this occurs immediately after rapid filling of the ventricles-3rd sound). It is rarely heard in normal adults because it is usually only heard under circumstances when pressures at high (systemic hypertension) or the ventricle is stiff, as is found in conditions such as ventricular hypertrophy.
What is automaticity of the heart?
The heart has the ability to initiate its own contraction without any outside stimulation. This property, known as *automaticity*, occurs due to "leaky" cell membranes, in which sodium and calcium ions slowly leak into the cells. This leaking causes the cell to slowly reach threshold, creating an action potential and initiating contraction. Following repolarization of the heart the cell membranes continue to leak and the cell moves toward threshold again. The result is a self-initiated stimulation that occurs at regular intervals (automaticity or rhythmicity). Heart rate is essentially dependent upon the rate of diffusion of sodium and calcium into the SA node cells.
What are the two parts of the heart?
The human heart actually functions as two separate pumps. 1) The right heart pumps blood into the *pulmonary circulation* and 2) the left heart pumps blood through the *systemic circulation*. Each side of the heart has two chambers. The *atria* receive blood from the *vena cava*, pulmonary veins, and cardiac veins. The *ventricles* receive blood from the atria and pump it out into the systemic and pulmonary circulation. In the human heart, the atrium and ventricle on the right side of the heart are separated from the atrium and ventricle on the left side by septa (*interatrial septum* and *interventricular septum*).