Exam 3 Flashcards
Hematocrit
The percentage of the blood volume that consists of red blood cells
Males: 42–52%
Females: 37–47%
Blood
Is a specialized connective tissue which contains cellular and liquid components: blood cells - formed elements (erythrocytes, leukocytes, platelets), plasma - fluid portion
Blood (circulatory system) function
Transportation, regulation, protection
Blood transportation
Carries respiratory gases, metabolites, Nutrients
Blood regulation
hormonal, temperature
Blood protection clotting
the circulatory system protects against blood loss from injury and foreign microbes or toxins introduced into the body.
blood protection immune
the immune function of the blood is performed by the leukocytes that protect against many disease
blood volume male and female
Male: 5-6 liters Female: 4-5 liters
plasma proteins
albumin, globulins, fibrinogen
Albumin
(60-80%) they are produced by the liver and provide the osmotic pressure needed to draw water from the surrounding tissue fluid into the capillaries
Globulins
(Alpha, beta, gamma. Alpha, beta are produced by the liver and function in transporting lipids and fat-soluble vitamins and function in immunity)
Fibrinogen
Is an important clotting factor produced by the liver. The fluid from clotted blood, called serum
Erythrocytes (red blood cells)
It contains 280 million hemoglobin molecules (gives blood its red color); Originate in the bone marrow
Each hemoglobin molecules consists of
four protein chains called globin’s, each of which is bound to one heme, a red-pigmented molecule that contains iron, the iron group of heme is able to combines with oxygen in the lungs and release oxygen in the tissues
Production of RBCs
Is mainly controlled by a hormonal mechanism. Cellular O2 deficiency is the initiating event in the production and release of the hormone erythropoietin (90% is produced in the glomeruli of the kidney, the rest mainly in the liver). Which stimulates red cell production in the bone marrow.
Leukocytes (White blood cells)
It contains nuclei and mitochondria and can move in an amoeboid fashion. Because of this can squeeze through pores in capillary walls and move to a site of infection (Diapedesis or extravasation).
Types of white blood cells
Agranular leukocytes (Lymphocytes, Monocytes), Granular leukocytes (eosinophils, basophils, neutrophils)
Lymphocytes
Compose 20–45% of WBCs
The most important cells of the immune system, their nucleus stains dark purple
Effective in fighting infectious organisms, Act against a specific foreign molecule (antigen)
Two main classes of lymphocyte
T cells, B cells
T cells
attack foreign cells directly
B cells
multiply to become plasma cells, secrete antibodies
Monocytes (e)
compose 4–8% of WBCs
The largest leukocytes, Are phagocytic cells
Nucleus: kidney shaped
Transform into macrophages
Platelets (Thrombocytes)
Blood clotting, by releasing serotonin, which stimulates constriction of the blood vessels, reducing the flow of blood to the injured area
Platelets also secrete growth factors, autocrine regulators
RBC life span
120 days
Aged RBCs
are removed from the blood in sinuses of the spleen and are degraded
Erythropoietin
Erythropoiesis refers to the formation of erythrocytes, and leukopoiesis to the formation of leukocytes
Hematopoiesis
HP give rise to blood cells originate in the yolk sac of the human embryo and then migrate to the liver of the fetus. The stem cells then migrate to the bone marrow.
These processes occur in two classes of tissues after birth, myeloid and lymphoid.
Myeloid tissue
is the red bone marrow of the long bones, sternum, pelvis, bodies of the vertebrae
Lymphoid tissue
includes the lymph nodes, tonsils, spleen, and thymus
The bone marrow produces
all of the different types of blood cells
Three factors for formation of erythrocyte
The production of red blood cells and synthesis of hemoglobin depends on the supply of iron, Vitamin B12, folic acid
Blood disorders
Anemia, leukemia, sickle cell disease
Sickle cell disease
Inherited blood disorder that affects red blood cells
People with sickle cell disease contain what in their RBC’s
mostly hemoglobin* S, an abnormal type of hemoglobin
The RBC’s of people with sickle cell sometimes become
sickle-shaped (crescent shaped) and have difficulty passing through small blood vessels
Sickle cells are destroyed rapidly in the body of people with
the disease causing anemia, jaundice and the formation of pigment gallstones
Almost all patients with sickle cell anemia have
painful episodes (crises), which can last from hours to days. These crises can affect the bones of the back, the long bones, and the chest
Sickle cell symptoms
Attacks of abdominal pain, Bone pain, Breathlessness, Delayed growth and puberty, Fatigue, Fever, Jaundice, Paleness, Rapid heart rate, Ulcers on the lower leg
Sickle cell treatment
They should take supplements of folic acid.
Antibiotics and vaccines are given to prevent bacterial infections
Hemoglobin
Is the main substance of the red blood cell
Hemoglobin helps RBC’s
carry oxygen from the air in our lungs to all parts of the body
Normal red blood cells contain
hemoglobin A, are soft and round and can squeeze through tiny blood tubes (vessels).
Normally, red blood cells live
for about 120 days before new ones replace them
Abnormal types of hemoglobin
Hemoglobin S and hemoglobin C
Leukemia
Is cancer of the blood cells
Leukemia starts
in the bone marrow, the soft tissue inside most bones
Bone marrow is where
blood cells are made
With leukemia, the bone marrow starts
to make a lot of abnormal white blood cells, called leukemia cells
leukemia cells
They don’t do the work of normal white blood cells, they grow faster than normal cells, and they don’t stop growing when they should
Type of luekemia
acute or chronic, lymphocytic, myelogenous
Lymphocytic (or lymphoblastic) leukemia affects
white blood cells called lymphocytes
Lymphocytic (or lymphoblastic) leukemia produces
large numbers of mature white blood cells (lymphocytes)
Myelogenous leukemia affects
white blood cells called myelocytes
Myelogenous leukemia produces
large numbers of immature and mature white blood cells (myelocytes).
Leukemia symptoms
Fever and night sweats, Headache, Bleeding easily, Bone or joint pain, Swollen lymph nodes in the armpit, neck, getting a lot of infections, Weakness, Losing weight
Leukemia treatments
chemotherapy, interferon-alpha (INFa) therapy, radiation therapy, stem cell transplantation (SCT)
Leukemia treatment Step 1
Chemotherapy - to kill leukemia cells using strong anti-cancer drugs
Leukemia treatment Step 2
Interferon-alpha (INFa) therapy - to slow the reproduction of leukemia cells and promote the immune system’s anti-leukemia activity
Leukemia treatment Step 3
Radiation therapy - to kill cancer cells by exposure to high-energy radiation.
Leukemia treatment Step 4
Stem cell transplantation - to enable treatment with high doses of chemotherapy and radiation therapy.
Types of blood vessels
arteries, capillaries, veins
Arteries
Carry blood away from the heart
Types of arteries
elastic arteries, muscular (distributing) arteries, arterioles
Elastic arteries
the largest arteries, High elastin, Diameters range from 2.5 cm to 1 cm (aorta and its major branches)
elastic arteries are also called
conducting arteries
Arterioles
smallest arteries
Veins
Carry blood toward the heart
veins conduct
blood from capillaries toward the heart
The blood pressure in veins
is much lower than in arteries
Venules
Smallest veins, diameters from 8-100 µm
Postcapillary venules
Smallest venules, venules join to form veins
Tunica externa
is the thickest tunic in veins
Some veins particularly in the limbs
have valves
Skeletal muscle pump
muscle press the veins and push the blood toward heart
Vascular anastomoses
surgical procedure connecting blood vessels together
Vasa vasorum
small blood vessels that supply the walls of larger blood vessels
Capillaries
Smallest blood vessels, the site of exchange of molecules between blood and tissue fluid
Capillaries diameter
from 8–10 µm
In capillaries, RBC’s pass
through single file
Capillary bed
Network of capillaries running through tissues
Low permeability capillaries
Blood-brain barrier
Highly selective, only vital substances pass through.
Not a barrier against O2, CO2 and some anesthetics
Sinusoids
Wide, leaky capillaries found in spleen, liver
Circulation through the heart Step 1
After flowing through the body, blood enters the heart at the right atrium
Circulation through the heart Step 2
From the right atrium, it passes through the right atrioventricular valve and into the right ventricle
Circulation through the heart Step 3
When the right ventricle contracts, it ejects the blood out of the heart through the pulmonary valve and into the pulmonary artery to the lungs
Circulation through the heart Step 4
After passing through the lungs, removing CO2 and picking up oxygen (O2), the blood returns through the pulmonary vein to the left atrium
Circulation through the heart Step 5
From here the blood enters the left ventricle through the left atrioventricular valve
Circulation through the heart Step 6
When the left ventricle contracts, blood is ejected through the aortic valve into the aorta and out to the body
Systemic circulation
the portion of the cardiovascular system which carries oxygenated blood away from the heart, to the body, and returns deoxygenated blood back to the heart. The term is contrasted with pulmonary circulation.
Systemic circulation Step 1
Oxygenated blood from the lungs leaves the left heart through the aorta, from where it is distributed to the body’s organs and tissues, which absorb the oxygen, through a complex network of arteries, arterioles, and capillaries
Systemic circulation Step 2
The deoxygenated blood is then collected by venules, from where it flows first into veins, and then into the inferior and superior venae cavae, which return it to the right heart, completing the systemic cycle
Systemic circulation Step 3
The blood is then re-oxygenated through the pulmonary circulation before returning again to the systemic circulation
Pulmonary circulation
is the portion of the cardiovascular system which carries oxygen-depleted blood away from the heart, to the lungs, and returns oxygenated blood back to the heart. The term is contrasted with systemic circulation
Pulmonary circulation Step 1
Oxygen-depleted blood from the body leaves the right heart through the pulmonary arteries, which carry it to the lungs, where red blood cells release carbon dioxide and pick up oxygen during respiration
Pulmonary circulation Step 2
The oxygenated blood then leaves the lungs through the pulmonary veins, which return it to the left heart, completing the pulmonary cycle
Pulmonary circulation Step 3
The blood is then distributed to the body through the systemic circulation before returning again to the pulmonary circulation
Hemodynamics: arteries
deliver oxygenated blood to the tissues, are thick-walled with extensive elastic tissue and smooth muscle, are under high pressure
hemodynamics: stressed volume
The blood volume contained in the arteries
Hemodynamics: arterioles are
the smallest branches of the arteries, the site of highest resistance in the cardiovascular system
Hemodynamics: arterioles have
a smooth muscle wall that is extensively innervated by autonomic nerve fibers
Hemodynamics: arteriolar resistance
is regulated by the autonomic nervous system (ANS)
Hemodynamics: Alpha1-Adrenergic receptors are found on the
arterioles of the skin, splanchnic, and renal circulations
Hemodynamics: Beta2-Adrenergic receptors are found on
arterioles of skeletal muscle
Hemodynamics: capillaries
consist of a single layer of endothelial cells surrounded by basal lamina, are thin-walled, are the site of exchange of nutrients, water and gases
Hemodynamics: Venules
are formed from merged capillaries
Hemodynamics: veins
progressively merge to from larger veins, are thin-walled, are under low pressure, contain the highest proportion of the blood in the cardiovascular system, have alpha 1-adrenergic receptors
Hemodynamics: vena cava
largest vein, returns blood to the heart
Hemodynamics: unstressed volume
The blood volume contained in the veins
Velocity
is directly proportional to blood flow and inversely proportional to the cross-sectional area at any level of the cardiovascular system.
Blood flow: the pressure gradient (P)
drives blood flow
Blood flows from
high pressure to low pressure
Blood flow
is inversely proportional to the resistance of the blood vessels
Resistance
is directly proportional to the viscosity of the blood and to the length of the vessel
Capacitance
Describes the distensibility of blood vessels
Is inversely related to elastance. The greater the amount of elastic tissue in a blood vessel, the higher the elastance, and the lower the compliance
Is directly proportional to volume and inversely proportional to pressure
Describes how volume changes in response to a change in pressure
Is much greater for veins than for arteries. As a result, more blood volume is contained in the veins (unstressed volume) than in the arteries (stressed volume).
Changes in the capacitance of the veins
produce changes in unstressed volume. For example, a decrease in venous capacitance decreases unstressed volume increases stressed volume by shifting blood from the veins to the arteries.
Capacitance of the arteries decreases
with age, as a person ages, the arteries become stiffer and less distensible
Mean pressure in the systemic circulation are as follows:
Aorta, 100 mm Hg
Arterioles, 50 mm Hg
Capillaries, 20 mm Hg
Vena cava, 4 mm Hg
Blood pressure
Is a force exerted by circulating blood on the walls of blood vessels
is not constant during a cardiac cycle. It is pulsatile
Systolic pressure
Is the highest arterial pressure during a cardiac cycle
Is measured after the heart contracts (systole) and blood is ejected into the arterial system
Diastolic pressure
Is the lowest arterial pressure during a cardiac cycle.
Is measured when the heart relaxed (diastole) and blood is returning to the heart via the veins
Pulse pressure
Is the difference between the systolic and diastolic pressures
The most important determinant of pulse pressure
stroke volume
As blood is ejected from the left ventricle into the arterial system
systolic pressure increases because of the relatively low capacitance of the arteries.
Because diastolic pressure remains unchanged during ventricular systole
the pulse pressure increases to the same extent as the systolic pressure
Decreases in capacitance, such those that occur with the aging process, cause
increases in pulse pressure
Mean arterial pressure
Can be calculated approximately as diastolic pressure plus one-third of pulse pressure
Venous pressure
Is very low, The veins have a high capacitance and therefore, can hold large volumes of blood at low pressure
Atrial pressure
Is even lower than venous pressure
Left atria pressure is estimated by
the pulmonary wedge pressure. A catheter, inserted into the smallest branches of the pulmonary artery, makes almost direct contact with the pulmonary capillaries. The measured pulmonary capillary pressure is approximately equal to the left atrial pressure
hypertension
Primary or essential hypertension is of unknown etiology.
Secondary hypertension
Primary hypertension: Environmental factors (dietary Na+, obesity, and stress), whatever the responsible pathogenic mechanisms, must lead to
Primary hypertension: increased total peripheral vascular resistance (TPR) by inducing vasoconstriction or to increased cardiac output (CO), or both
Primary hypertension: Sympathetic nervous system and renin-angiotensin-aldosteron system have received the most attention for
the pathophysiology of hypertension, both can increase CO and TPR
Primary hypertension: Abnormal Na+ transport across the cell wall due to a
defect in or inhibition of the Na+/K+ pump or because of increased permeability to the Na+
Primary hypertension: Increased intracellular Na+
which makes the cell more sensitive to sympathetic stimulation
Primary hypertension: Since Ca2+ follows Na+, accumulation of intracellular Ca2+ is responsible for
the increased sensitivity
Deficiency of a vasodilator substance
prostaglandin, bradykinin
Secondary hypertension
Can be caused by conditions that affect your kidneys, arteries, heart or endocrine system. Secondary hypertension can also occur during pregnancy, disorders of the adrenal gland, thyroid and parathyroid problems
Cushings syndrome (second hypertension)
a condition caused by an overproduction of cortisol
Hyperaldosteronism (second hypertension)
too much aldosterone
Pheuchromocytoma (second hypertension)
a rare tumor that causes over secretion of hormones like adrenaline and NA
Kidney disease (second hypertension)
polycystic kidney disease, kidney tumor, kidney failure, or a narrow or blocked main artery supplying the kidney
Drugs such as (second hypertension)
corticosteroids (anti-inflammatory drugs like prednisone) leads to increased systolic, diastolic pressures and increases arterial resistance. Nonsteriodal anti-inflammatory drugs (motrin, aleve), weight loss drugs (such as meridia), salt and water retention, sympathetic activity, loss of renal vasodilation
coarctation of the aorta (second hypertension)
a birth defect in which the aorta is narrowed
preclampsia (second hypertension)
a condition related to pregnancy, endothelial dysfunction in the maternal blood vessels
Hypertension symptoms
Usually asymptomatic, Headache, Fatigue, Shortness of breath, Dizziness, Convulsion, Changes in vision (Blurred vision, Double vision), Nausea, Vomiting, Anxiety, Increased sweating, Nose bleeds, Tinnitus - ringing or buzzing in ears, Heart palpitations, General feeling of unwellness, Increased urination frequency, flushed face, Pale skin
Hypertension treatment
Angiotensin-converting enzyme (ACE) inhibitors: Captopril, Ramipril
Angiotensin II receptor blockers (ARBs): Valsartan
Diuretics: Thiazide diuretics such as hydrochlorothiazide
Calcium channel blockers: Felodipine, Benidipine
Beta-adrenergic blocking agents: Propranolol
P Wave represents
the wave of depolarization that spreads from the SA node throughout the atria, and is usually 0.08 to 0.1 seconds (80-100 ms) in duration (atrial depolarization)
P Wave does not include
atrial repolarization, which is buried in the QRS complex
PR Interval
The period of time from the onset of the P wave to the beginning of the QRS complex, which normally ranges from 0.12 to 0.20 seconds in duration
PR interval represents
the time between the onset of atrial depolarization and the onset of ventricular depolarization.
If the PR interval is greater than
0.2 sec, there is an AV conduction block
QRS complex
The duration of the QRS complex is normally 0.06 to 0.1 seconds. This relatively short duration indicates that ventricular depolarization normally occurs very rapidly
If the QRS complex is prolonged, greater than
0.1 sec, conduction is impaired within the ventricles. This can occur with bundle branch blocks or whenever a ventricular foci (abnormal pacemaker site) becomes the pacemaker driving the ventricle
Ectopic foci are
abnormal pacemaker sites within the heart (outside of the SA node) that display automaticity
Such an ectopic foci nearly always results in
impulses being conducted over slower pathways within the heart, thereby increasing the time for depolarization and the duration of the QRS complex
ST segment
Is the segment from the end of the S wave to the beginning of the T wave
ST segment represents
the period when the ventricles completely are depolarized
ST segment important in the diagnosis of? Why?
ventricular ischemia or hypoxia because under those conditions, the ST segment can become either depressed or elevated
T Wave represents
ventricular repolarization and is longer in duration than depolarization (i.e., conduction of the repolarization wave is slower than the wave of depolarization).
What may be seen following the T wave
Sometimes a small positive U wave may be seen. This wave represents the last remnants of ventricular repolarization
Inverted or prominent U waves indicates
underlying pathology or conditions affecting repolarization
QT Interval
Is the interval from the beginning of the Q wave to the end of the T wave.
QT interval represents
the time for both ventricular depolarization and repolarization to occur, and therefore roughly estimates the duration of an average ventricular action potential. Represents the entire period of depolarization and repolarization of the ventricles
QT interval can range from
0.2 to 0.4 seconds depending upon heart rate
At high heart rates
ventricular action potentials shorten in duration, which decreases the Q-T interval Because prolonged Q-T intervals can be diagnostic for susceptibility to certain types of tachyarrhythmias.
Ventricles, atria and the purkinje system have
resting membrane potentials of about -90mV. This value approaches the K+ equilibrium potential
Action potential are of
long duration, especially in Purkinje fibers, where they last 300 msec
Cardiac Action Potential Phase 0
Is the upstroke of the action potential
Is caused by a transient increase in Na+ conductance. This increase results in an inward Na+ current that depolarizes the membrane
At the peak of the action potential, the membrane potential approaches the Na+ equilibrium potential
Cardiac Action Potential Phase 1
Is a brief period of initial repolarization
Initial repolarization is caused by an outward current, in part because of the movement of K+ ions (favored by both chemical and electrical gradients) out of the cell and in part because of a decrease in Na+ conductance
Cardiac Action Potential Phase 2
Is the plateau of the action potential
Is caused by a transient increase in Ca2+ conductance, which results in an inward Ca2+ current, and by an increase in K+ conductance.
During phase 2, outward and inward currents are approximately equal, so the membrane potential is stable at the plateau level
Cardiac Action Potential Phase 3
Is repolarization.
During phase 3, Ca2+ conductance decreases, and K+ conductance increases and therefore predominates.
The high K+ conductance results in a large outward K+ current (Ik) which hyperpolarizes the membrane back toward the K+ equilibrium potential
Cardiac Action Potential Phase 4
Is the resting membrane potential.
Is a period during which inward and outward current (Ik1) are equal and the membrane potential approaches the K= equilibrium potential
Sinoatrial node
Is normally the pacemaker of the heart
Has an unstable resting potential
Sinoatrial node Phase 0
Is upstroke of the action potential
Is caused by an increase in Ca2+ conductance. This increase causes an inward Ca2+ current that drives the membrane potential toward the Ca+ equilibrium potential.
The ionic basis for phase 0 in SA node is different from that in the ventricles, atria and Purkinje fibers (where it is result of an inward Na+ current.)
Sinoatrial node Phase 1-2
Are not present in the SA node action potential
Sinoatrial node Phase 3
Is repolarization
Is caused by an increase in K+ conductance. This increase results in an outward K+ current that causes repolarization of the membrane potential
Sinoatrial node Phase 4
Is slow depolarization.
Accounts for the pacemaker activity of the SA node (automaticity).
Is caused by an increase in Na+ conductance, which results in an inward Na+ current called If (slow depolarization, produced by the opening of Na+ channels and an inward Na+ current called If). (“f” which stands for funny)
AV node
Upstroke of the action potential in the AV node is the result of an inward Ca+ current (as in the SA node)
Conduction velocity
Reflects the time required for excitation to spread throughout cardiac tissue.
Conduction velocity depends
on the size of the inward current during the upstroke of the action potential. The larger the inward current the higher the conduction velocity.
Is conduction velocity the slowest or the fastest in the purkinje system
is the fastest in the purkinje system
Conduction velocity is the slowest in?
the AV node, allowing time for ventricular filling before ventricular contraction. If conduction velocity through the AV node is increased, ventricular filling may be compromised.
Excitability
Is the ability of cardiac cells to initiate action potentials in response to inward, depolarizing current
Excitability reflects
the recovery of channels that carry the inward currents for the upstroke of the action potential.
Excitability changes
over the course of the action potential. These changes in excitability are described by refractory periods
Absolute refractory period (ARP)
No action potential can be initiated (absolute means absolutely no stimulus is large enough to generate another action potential)
Effective refractory period (ERP)
ERP is slightly longer than (effective means that a conducted action potential cannot be generated)
Relative refractory period (RRP)
Action potential can be elicited but more than the usual inward current is required.
RRP begins at the
end of the absolute refractory period and continues until the cell membrane has repolarized to about -70mV
During RRP it is possible
to generate a second action potential (which is an abnormal configuration and shortened plateau phase)
Chronotropic effects
produces changes in heart rate
A negative chronotropic effect
decreases heart rate by decreasing the firing rate of the SA node.
A positive chronotropic effect
increases heart rate by increasing the firing rate of the SA node
Dromotropic effect
Produce changes in conduction velocity, primarily in the AV node.
Dromotropic effect decreases
conduction velocity through the AV node, slowing the conduction of action potentials from the atria to the ventricles and increasing the PR interval.
A positive dromotropic effect
increases conduction velocity through the AV node, speeding the conduction of action potentials from the atria to the ventricles and decreasing the PR interval
A negative inotropic effect
decreases force of contraction, a positive inotropic effect increases force of contraction
At rest, a normal heart beats around
50 to 99 times a minute
Arrhythmias
It results from abnormalities in impulse formation or in impulse conduction, Disturbances in the formation of impulses lead to change in the sinus rhythm
Sinus tachycardia
If sinus frequency rises above 100/min (exercise, psychic excitation, fever, rise of 10 beats/min
Sinus bradycardia
If it drops below 50-60/min. In both cases the rhythm is regular
Atrial Tachycardia
A rhythm disturbance that arises in the atria
Heart rates during atrial tachycardia are
highly variable, with a range of 100-250 beats per minute (bpm). The atrial rhythm is usually regular
Ventricular Tachycardia
It results from a rapid sequence of ectopic ventricular impulses. Beginning with ES
Ventricular filling, cardiac output, ventricular fibrillation (Ventricular Tachycardia)
Ventricular filling and cardiac output decrease and ventricular fibrillation can even ensue, that is a high frequency uncoordinated twitching of the myocardium
Unless ventricular tachycardia is treated
the failure to eject blood can be just as dangerous as cardiac arrest. With a rate between 120 and 250 beats per minute
Supraventricular arrhythmia
atrial or nodal extrasystole (ES). Abnormal or ectopic (heterotopic) impulses may arise in the atria (atrial), in the AV node (nodal) or in the ventricle (ventricular).
The impulses from an atrial (or nodal) ectopic focus are
transmitted to the ventricle, which thus thrown out of its sinus rhythm: supraventricular arrhythmia due to atrial or nodal extrasystole (ES).
In atrial ES the P wave is
deformed but the QRS complex is normal.
In nodal extrasystole, stimulation of the
atria is retrograde; the P wave is thus negative and is either masked by the QRS wave or appears shortly after it. Because in supraventricular extrasystole the sinus nodes often also depolarize.
Ventricular extrasystole (infranodal extrasystole)
Ventricular premature complexes (VPCs) are ectopic impulses originating from an area distal to the His Purkinje system
Ventricular premature complexes (VPCs) are the
most common ventricular arrhythmia, in this case the QRS complex of the ES is deformed
Two common mechanisms exist for VPCs
automaticity, reentry
Automaticity
This is the development of a new site of depolarization in nonnodal ventricular tissue, which can lead to a VPC
Increased automaticity could be due to
electrolyte abnormalities or ischemic myocardium.
Reentry circuit
Reentry typically occurs when slow-conducting tissue (eg, infarcted myocardium) is present adjacent to normal tissue
The slow conducting tissue from reentry circuit could be due to
damaged myocardium, as in the case of a healed MI
Premature ventricular contraction (ventricular extrasystole) possible causes
Ischemia, Certain medicines such as digoxin, which increases heart contraction, Myocarditis, Cardiomyopathy hypertrophic or dilated, Hypoxia, Hypercapnia (CO2 poisoning), Mitral valve prolapse, Smoking, Alcohol, Drugs such as cocaine, Caffeine, Magnesium and potassium deficiency, Calcium excess, Thyroid problems, Heart attack
Premature ventricular contraction (ventricular extrasystole) symptoms
Chest pain, Faint feeling, Fatigue, Hyperventilation (after exercise)
Frequent episodes of continuous premature ventricular contraction (PVCs) becomes a form of
ventricular tachycardia (VT), which is a rapid heartbeat, because there is an extra electrical impulse, causing an extra ventricular contraction.
Treatment of ventricular extrasystole (premature ventricular contraction) (PVC)
Restoring the balance of magnesium, calcium and potassium within the body
Class I agents
Sodium channel blockers. Class I agents are grouped by what effect they have on the Na+ channel, and what effect they have on cardiac action potentials. Lidocaine, Phenytoin
Class II agents
Beta blockers. They act by blocking the effects of catecholamines at the β1-adrenergic receptors, thereby decreasing sympathetic activity on the heart. They decrease conduction through the AV node. Class II agents include atenolol, propranolol, and metoprolol
Class III agents
Block the potassium channels, thereby prolonging repolarization. Since these agents do not affect the sodium channel, conduction velocity is not decreased. Sotalol
Class IV agents
Calcium channel blockers. They decrease conduction through the AV node, and shorten phase two (the plateau) of the cardiac action potential. They thus reduce the contractility of the heart, so may be inappropriate in heart failure. However, in contrast to beta blockers, they allow the body to retain adrenergic control of heart rate and contractility. Class IV agents include verapamil and diltiazem
AV node block
PR interval in the normal heart, this time is 0.12 to 0.20 second in duration, damage to AV node causes slowing of impulse conduction and is reflected by changes in the PR interval
First degree AV node block
PR interval exceeds 0.20 second
Second degree AV node block
Occurs when the AV node is damaged so severely that only one out of every two, three, or four atrial electrical waves can pass through to the ventricles.
ECG: P waves without associated QRS waves
Third-degree, or complete, AV node block
none of the atrial waves can pass through the AV node to the ventricles. Result is bradycardia
Excitation-contraction Step 1
The action potential (AP) spreads from the cell membrane into the T tubules
Excitation-contraction Step 2
During the plateau of AP, Ca2+ conductance is increased and Ca2+ enters the cell from extracellular fluid (inward Ca2+ current).
Excitation-contraction Step 3
This Ca2+ entry triggers the release of even Ca2+ from the SR (Ca2+ induced Ca2+ release).
Excitation-contraction Step 4
As a result of this Ca2+ release, intracellular (Ca2+) increases
Excitation-contraction Step 5
Ca2+ binds to troponin C, and tropomyosin is moved out of the way, removing the inhibition of action and myosin binding
Excitation-contraction Step 6
Actin and myosin binds, the thick and thin filaments slide past each other, and the myocardial cell contracts
Excitation-contraction Step 7
Relaxation occurs when Ca2+ is reaccumulated by the SR by an active Ca2+-ATPase pump
Contractility
Is the intrinsic ability of the cardiac muscle to develop force at a given muscle length. It is also called inotropism.
Is related to the intracellular Ca2+ concentration.
Contractility is estimated by
the ejection fraction (stroke volume/end-diastolic volume), which is normally 0.55 (55%).
Positive inotropic agents produce
an increase in contractility
Negative inotropic agents produce
a decrease in contractility
Factors that increase contractility (positive inotropism)
Increased heart rate, sympathetic stimulation, cardiac glycoides (digitalis)
Increased heart rate
More AP occur per unit time, more Ca2+ enters the myocardial cells during the AP plateaus, more Ca2+ is released from the SR, and greater tension is produced during contraction.
Sympathetic stimulation
Increases the inward Ca2+ current during the plateau of each cardiac action potential.
It increases the activity of the Ca2+ pump of the SR as a result more Ca2+ is accumulated by the SR and thus more Ca2+ is available for release in subsequent beats.
Factors that decrease contractility (negative inotropism)
Parasympathetic (Ach) via muscarinic receptors: decrease the force of concentration in the atria by decreasing the inward Ca2+ current during the plateau of the cardiac action potential
Length-tension relationship in the ventricles
Preload, afterload, sarcomere length, velocity of contraction at a fixed muscle length
Preload
is equivalent to end-diastolic volume, which is related to right atrial pressure.
When venous return increases, end-diastolic volume increases and stretches or lengthens the ventricular muscle fibers
Left ventricle (afterload)
is equivalent to aortic pressure. Increases in aortic pressure cause an increase in afterload on the left ventricle
Right ventricle (afterload)
is equivalent to pulmonary artery pressure
Increases in pulmonary artery pressure (afterload)
cause an increase in afterload on the right ventricle.
Sarcomere length determines
the maximum number of cross-bridges that can form between actin and myosin. the maximum tension, or force of contraction.
Velocity of contraction at a fixed muscle length
is maximal when the afterload is zero, is decreased by increases in afterload.
Frank-starling relationship describes
the increases in stroke volume and cardiac output that occur in response to an increase in venous return or end-diastolic volume
Frank-starling relationship is based
on the length-tension relationship in the ventricle. Increases in end-diastolic volume cause an increase in ventricular fiber length, which produces an increase in developed tension.
Frank-starling relationship is the mechanism
that matches cardiac output to venous return. The greater the venous return, the greater the cardiac output.
Changes in contractility shift the Frank-Starling curve
upward (increased contractility) or downward (decreased contractility).
Increases in contractility cause an
increase in cardiac output for any level of right atrial pressure or end-diastolic volume
Decreases in contractility cause a
decrease in cardiac output for any level of right atrial pressure or end-diastolic volume
Cardiac cycle
Isovolumetric ventricular contraction, Ventricular systole, Early ventricular diastole, Late ventricular diastole (ventricular filling)
Step (1-2)—Isovolumetric ventricular contraction
Also called early ventricular systole. This begins with the ventricles depolarizing (QRS complex) then contracting. The left ventricle is filled with blood from the left atrium and its volume is about 140 ml (end-diastolic volume). Ventricular pressure is low because the ventricular muscle is relaxed.
Step (1-2)—Isovolumetric ventricular contraction, on excitation
the ventricle contracts and ventricular pressure increases. The mitral valve closes when left ventricular pressure is greater than left atrial pressure. Because all valves are closed, no blood can be ejected from the ventricle (isovolumetric).
Step (2- 3) Ventricular systole
Also called ejection period. The aortic valve opens at point 2 when pressure in the left ventricle exceeds pressure in the aorta. Blood is ejected into the aorta, and ventricular volume decreases. The volume that is ejected in this phase is the stroke volume. The volume remaining in the left ventricle at point 3 is end-systolic volume
Step (3-4)—Early ventricular diastole
Also called isovolumetric relaxation phase. At point 3, the ventricle relaxes. When ventricular pressure decreases to less than aortic pressure, the aortic valve closes. Because all of the valves are closed again, ventricular volume is constant (isovolumetric) during this phase.
Step (4-1)— Late ventricular diastole (ventricular filling)
Once left ventricular pressure decreases to less than left atrial pressure, the mitral (AV) valve opens and filling of the ventricle begins. During this phase, ventricular volume increases to about 140 ml (the end-diastolic volume)
Changes in ventricular pressure-volume loop are caused by several factors
increased preload, increased afterload, increased contractility
Increased preload
refers to an increase in end-diastolic volume and is the result of increased venous return.
increased preload causes
an increase in stroke volume based on the Frank-Starling relationship.
The increased in stroke volume caused by increased preload
is reflected in increased width of the pressure-volume loop.
Increased afterload
refers to an increase in aortic pressure.
The ventricle must eject blood against a higher pressure, resulting in a decrease in stroke volume.
The decrease in stroke volume from increased afterload
is reflected in decreased width of the pressure-volume loop. results in an increase in end-systolic volume.
Increased contractility
The ventricle develops greater tension than usual during systole, causing an increase in stroke volume.
The increase in SV results in a decrease in end-systolic volume.
Stroke volume
is the volume ejected from the ventricle on each beat.
Stroke volume= End-diastolic volume - End-systolic volume
Cardiac output
Cardiac output (CO) is the amount of blood each ventricle can pump in one minute
CO= Stroke volume x Heart rate
Cardiac output is distributed among various organs:
Cerebral=15%, Coronary=5%, Renal=25%, Gastrointestinal=25%, Skeletal muscle=25%, Skin=5%
Ejection fraction
Is the fraction of the end-diastolic volume ejected in each stroke volume. Is related to contractility. Is normally 0.55, or 55%.
EF = Stroke volume/End-diastolic volume
Cardiac O2 consumption
Is directly related to the amount of tension developed by the ventricles
cardiac O2 consumption is increased by
Increased afterload (increased aortic pressure), Increased size of the heart, Increased contractility, Increased heart rate
Measurement of cardiac output by the Fick principle:
CA (Cardiac output) = O2 consumption/O2 pulmonary vein-O2 pulmonary artery
The opening of heart valves
is a slowly developing process and produces no sound. However, when they close, the vanes of the valves and the surrounding fluid vibrate under the influence of sudden pressure differences, producing sounds that travel in all directions through the chest.
The first heart sound (lub)
is produced (indirectly) by the closure of the AV valves; it is of low pitch and of relatively long duration
The second heart sound (dup)
is produced (indirectly) by the closing of the aortic and pulmonary semilunar valves; this is of high pitch and of relatively smaller duration.
A third heart sound
sometimes occurs in the middle of diastole. This is caused by blood flowing with rumbling motion into the almost filled ventricles; it is difficult to hear with a stethoscope.
Atherosclerosis
is patchy intimal plaques (atheromas) in medium and large arteries; the plaques contain lipids, inflammatory cells, smooth muscle cells, and connective tissue
Artherosclerosis happens when
the arteries get blocked by fats and cholesterol
Atherosclerosis can affect
all large and medium-sized arteries, including the coronary, carotid, and cerebral arteries, the aorta, its branches, and major arteries of the extremities
the causes of Atherosclerosis
Dyslipidemia, diabetes, cigarette smoking, family history, sedentary lifestyle, obesity, and hypertension
The hallmark of atherosclerosis is the
atherosclerotic plaque, which contains lipids (intracellular and extracellular cholesterol and phospholipids), inflammatory cells (eg, macrophages, T cells), smooth muscle cells, connective tissue (eg, collagen, elastic fibers), thrombi, Ca++ deposits.
Atherosclerosis symptoms
Shortness of breath, Tightening pain in the chest
Atherosclerosis complications
Strokes, Damage of muscles, body organs and blood vessels, Deficiency of blood supply due to obstruction (angina)
Atrial fibrillation and flutter
are abnormal heart rhythms in which the atria are out of sync with the ventricles.
In atrial flutter
the atria beat regularly and faster than the ventricles.
In atrial fibrillation
the heart beat is completely irregular. The atrial muscles contract very quickly and irregularly; the ventricles beat irregularly but not as fast as the atria.
When the atria fibrillate
blood that is not completely pumped out can pool and form a clot. In atrial flutter, the heart beat is usually very fast but steady. The atria beat faster than the ventricles.
Atrial fibrillation often occurs in
people with various types of heart disease. Atrial fibrillation may also result from an inflammation of the heart’s covering (pericarditis), chest trauma or surgery, pulmonary disease, and certain medications
Atrial fribrillation and flutter causes and symptoms
many types of heart disease, stress and anxiety, caffeine, alcohol, tobacco, diet pills, open heart surgery
Heart murmurs
are generated by turbulent flow of blood, which may occur inside or outside the heart. Murmurs may be physiological (benign) or pathological (abnormal).
Abnormal murmurs can be caused by
Stenosis restricting the opening of a heart valve, causing turbulence as blood flows through it
Valve insufficiency (or regurgitation) allows backflow of blood when the incompetent valve is supposed to be closed.
ECG electrodes
There are three standard leads, usually designated as I, II and III. They are bipolar (i.e., they detect a change in electric potential between two points) and detect the electrical potential change in the frontal plane
Lead I
is between the right arm and left arm electrodes, the left arm being positive
Lead II
is between the right arm and left leg electrodes, the left leg being positive
Lead III
is between the left arm and left leg electrodes, the left leg again being positive
Chest Electrode Placement V1
Fourth intercostal space to the right of the sternum
Chest Electrode Placement V2
Fourth intercostal space to the Left of the sternum
Chest Electrode Placement V3
Directly between leads V2 and V4
Chest Electrode Placement V4
Fifth intercostal space at midclavicular line
Chest Electrode Placement V5
Level with V4 at left anterior axillary line
Chest Electrode Placement V6
Level with V5 at left midaxillary line (Directly under the midpoint of the armpit)
Chest Leads
V1 & V2, V3 & V4, V5 & V6
Chest leads view
Right Ventricle, Septum/Lateral Left Ventricle, Anterior/Lateral Left Ventricle
Myocardial infarction
The blood supply to certain areas of the myocardium is obstructed. The muscle tissue at the center of the infarct dies off
In atherosclerosis
plaque builds up in the walls of your coronary arteries. This plaque is made up of cholesterol and other cells. A heart attack can occur
Myocardial infarction
Stress, Male gender, Diabetes, Family history of coronary artery disease (genetic or hereditary factors), High blood pressure, Smoking, Unhealthy cholesterol levels especially high LDL (“bad”) cholesterol and low HDL (“good”) cholesterol, chronic kidney disease
Myocardial infraction symptoms
chest pain (angina pectoris), Sweating, Anxiety, Cough, Fainting, Dizziness, Nausea or vomiting, Palpitations (feeling like your heart is beating too fast), Dyspnea
Chest pain (angina pectoris)
Feeling the pain in only one part of your body, or it may move from your chest to your arms, shoulder, neck, teeth, jaw, belly area, or back
Chest pain (angina pectoris) The pain can be severe or mild. It can feel like
A tight band around the chest, Bad indigestion, something heavy sitting on your chest, Squeezing or heavy pressure, The pain usually lasts longer than 20 minutes. Rest and a medicine do not completely relieve the pain of a heart attack. Symptoms may also go away and come back
Myocardial infarction diagnostic criteria Step 1
Clinical history of ischaemic type chest pain lasting for more than 20 minutes
Myocardial infarction diagnostic criteria Step 2
Changes in serial ECG tracings
Myocardial infarction diagnostic criteria Step 3
Rise and fall of serum cardiac biomarkers such as creatine kinase -MB fraction and troponin T and I and myoglobin, Lactate dehydrogenase as they are more specific for myocardial injury. (The cardiac troponins T and I which are released within 4–6 hours of an attack of MI and remain elevated for up to 2 weeks)
Myocardial infarction diagnostic criteria Step 4
If there is a high positive R, there is also a Larger negative Q waves, ST segment elevation or depression, or coronary intervention are diagnostic of MI
Myocardial infarction management
A MI is a medical emergency which requires immediate medical attention. Oxygen, aspirin, and nitroglycerin.
Endocarditis
is inflammation of the inside lining of the heart chambers and heart valves (endocardium)
Endocarditis is usually a result
of a blood infection. Bacteria or other infectious substance can enter the bloodstream during certain medical procedures, including dental procedures, and travel to the heart, where it can settle on damaged heart valves. The bacteria can grow and may form infected clots that break off and travel to the brain, lungs, kidneys, or spleen
The following increase chances for developing endocarditis
Artificial heart valves, congenital heart disease (atrial septal defect, patent ductus arteriosus), Heart valve problems (such as mitral insufficiency), History of rheumatic heart disease
Endocarditis symptoms
Abnormal urine color, Chills (common), Excessive sweating (common), Fatigue, Fever (common), Joint pain, Muscle aches and pains, Night sweats, Nail abnormalities (splinter hemorrhages under the nails), Paleness
The following tests may be performed for endocarditis
Blood culture and sensitivity (to detect bacteria), Chest x-ray, Complete blood count (may show mild anemia), Echocardiogram (ultrasound of the heart), Erythrocyte sedimentation rate (ESR), Transesophageal echocardiogram
Endocarditis treatment
Long-term, high-dose antibiotic treatment is needed to get rid of the bacteria. Treatment is usually given for 4-6 weeks, depending on the specific type of bacteria. Blood tests will help your doctor choose the best antibiotic. Surgery may be needed to replace damage heart valves.
Mitral stenosis
is a heart valve disorder that involves the mitral valve. Stenosis refers to a condition in which the valve does not open fully, restricting blood flow
metro stenosis cause
the valve area becomes smaller, less blood flows to the body. The upper heart chamber swells as pressure builds up. Blood may flow back into the lungs. Fluid then collects in the lung tissue (pulmonary edema), making it hard to breathe, Rheumatic fever, Congenital mitral stenosis
mitral stenosis symptoms
May begin with an episode of: Atrial fibrillation, Chest discomfort (rare): Increases with activity, decreases with rest. Radiates to the arm, neck, jaw, or other areas. Tight, crushing, pressure. Cough possibly bloody (hemoptysis), Difficulty breathing during or after exercise or when lying flat; may wake up with difficulty breathing, Fatigue, becoming tired easily, Bronchitis, Palpitations, Swelling of feet or ankles
Mitral stenosis complications
Atrial fibrillation and atrial flutter, Blood clots to the brain (stroke), intestines, kidneys, or other areas, Heart failure, Pulmonary edema, Pulmonary hypertension
Mitral Stenosis (ECG)
There is atrial fibrillation. No P waves are visible. The rhythm is irregularly irregular (random). With severe pulmonary hypertension, right ventricular hypertrophy can be seen
Mitral Stenosis (ECG): Treatment
Cardiac Glycosides: These agents alter the electrophysiologic mechanisms responsible for arrhythmia, Digoxin (Lanoxin). Diuretics, β-blockers, Ca2+ channel blockers, Anticoagulants, balloon valvotomy, surgical commissurotomy, valve replacement
Digoxin: Negatively chronotropic
i.e., slowing the heart rate by decreasing conduction of electrical impulses through the AV node, making it a commonly used antiarrhythmic agent in controlling the heart rate during atrial fibrillation or atrial flutter.
Digoxin: Positively inotropic
i.e., increasing the force of heart contraction via inhibition of the Na+/K+ ATPase pump
Mitral Regurgitation
is a long-term disorder in which the heart’s mitral valve does not close properly, causing blood to flow backward (leak) into the upper heart chamber when the left lower heart chamber contracts. The condition is progressive, which means it gradually gets worse.
Mitral Regurgitation causes
Mitral valve prolapse, Congenital, Atherosclerosis, Endocarditis, Heart tumors, High blood pressure, Marfan syndrome, Untreated syphilis
mitral regurgitation symptoms
Cough, Fatigue, Palpitations (related to atrial fibrillation), Shortness of breath during activity and when lying down, Urination, excessive at night, enlarged liver
mitral regurgitation treatment
The choice of treatment depends on the symptoms present and the condition and function of the heart. antihypertensive drugs and vasodilators
Mitral regurgitation antibiotics
reduce the risk of infective endocarditis in patients with mitral valve prolapse who are having dental work.
mitral regurgitation anticogulant or antiplatelet medications
prevent clot formation in patients with atrial fibrillation.
mitral regurgitation digitalis
may be used to strengthen the heartbeat, along with diuretics to remove excess fluid in the lungs
Baroreceptor regulating of arterial pressure
Fast mechanism: neural, (baroreceptor)
Slow mechanism: hormonal (renin-angiotensin-aldosterone)
Baroreceptor reflex
includes fast, neural mechanisms.
is a negative feedback system that is responsible for the minute-to-minute regulation of arterial pressure.
Baroreceptors are
stretch receptors located within the walls of the carotid sinus near the bifurcation of the common carotid arteries.
Steps in the baroreceptor reflex Step 1
A decrease in arterial pressure decreases stretch on the walls of the carotid sinus. Because the baroreceptors are most sensitive to changes in arterial pressure, rapidly decreasing arterial pressure produces the greatest response. Additional baroreceptors in the aortic arch respond to increases, but not to decreases, in arterial pressure.
Steps in the baroreceptor reflex Step 2
Decreased stretch decreases the firing rate of the carotid sinus nerve cranial nerve IX, which carries information to the vasomotor center in the brain stem.
Steps in the baroreceptor reflex Step 3
The set point for mean arterial pressure in the vasomotor center is about 100 mm Hg. Therefore, if mean arterial pressure is less than 100 mm Hg, a series of autonomic responses is coordinated by the vasomotor center. These changes will attempt to increase blood pressure toward normal.
Steps in the baroreceptor reflex Step 4
The responses of the vasomotor center to a decrease in mean arterial blood pressure are coordinated to increase the arterial pressure to 100 mm Hg. The responses are decreased parasympathetic (vagal) outflow to the heart and increased sympathetic outflow to the heart and blood vessels
The following four effects attempt to increase the arterial pressure to normal:
Increases heart rate, Increases contractility and stroke volume, Increases vasoconstriction of arterioles, Increases vasoconstriction of veins
Example of the baroreceptor reflex:
response to acute blood loss
Renin angiotensin aldosterone
is a slow, hormonal mechanism, Regulation by adjustment of blood volume, Renin is an enzyme.
Angiotensin I
is inactive
Angiotensin II
is physiologically active, is degraded by angiotensinase
Renin angiotensin aldosterone Example
response of the RAA system to acute blood loss.
Other regulation of arterial blood pressure:
Cerebral ischemia, Chemoreceptors in the carotid and aortic bodies, Vasaopressin (antidiuretic hormone), Atrial natriuretic peptide (ANP)
Cerebral ischemia Step 1
Pco2 pressure increases in brain tissue
Cerebral ischemia Step 2a
Chemoreceptors in the vasomotor center respond by increasing sympathetic outflow to the heart and blood vessels
Cerebral ischemia Step 2b
Constriction of arterioles causes intense peripheral vasoconstriction and increased TPR.
Cerebral ishemia step 2c
Blood flow to other organs (kidneys) is significantly reduced in an attempt to preserve blood flow to the brain
Cerebral ishemia step 3a
The Cushing reaction in an example of the response to cerebral ischemia. Increases intracranial pressure cause compression of the cerebral blood vessels, leading to cerebral ischemia and increased cerebral Pco2.
Cerebral ishemia step 3b
The vasomotor center directs an increase in sympathetic outflow to the heart and blood vessels, which causes a profound increase in arterial pressure.
Chemoreceptors in carotid and aortic bodies
are located near the bifurcation of the common carotid arteries and along the aortic arch
Chemoreceptors in carotid and aortic bodies have
very high rates of O2 consumption and are very sensitive to decreases in the partial pressure of oxygen (Po2)
Chemoreceptors in carotid and aortic bodies decreases in
Po2 activate vasomotor centers that produce vasoconstriction, an increase in TPR, and an increase in arterial pressure.
Regulation by antidiuretic hormone (ADH) too little water in blood
Too little water in blood -> detected by hypothalamus -> more ADH secreted into blood by pituitary gland -> kidneys absorb less water from blood -> less urine produced -> blood water level back to normal
Regulation by antidiuretic hormone (ADH) too much water in blood
Too much water in blood -> detected by hypothalamus -> less ADH secreted into blood by pituitary gland -> kidneys absorb more water from blood -> lots of dilute urine produced -> blood water level back to normal
Atrial Natriuretic peptide (ANP) Physiological effects:
ANP binds to a specific set of receptors. Receptor-agonist binding causes a reduction in blood volume and therefore a reduction in cardiac output and systemic blood pressure.
Atrial Natriuretic peptide (ANP) inhibits
renin secretion, thereby inhibiting the renin-angiotensin system, Reduces aldosterone secretion by the adrenal cortex, Relaxes vascular smooth muscle in arterioles and venules.
Microcirculation and lymph Structure of capillary beds
At the junction of the arterioles and capillaries is a smooth muscle band called the precapillary sphincter.
Microcirculation and lymph Structure of capillary beds true capillaries
do not have smooth muscle; they consist of a single layer of endothelial cells surrounded by a basement membrane.
Microcirculation and lymph Structure of capillary beds clefts (pores)
between the endothelial cells allow passage of water-soluble substances. The clefts represent a very small fraction of the surface area (<0.1%).
Microcirculation and lymph Structure of capillary beds blood flow
Blood flow through the capillaries is regulated by contraction and relaxation of the arterioles and the precapillary sphincters.
Lymph (function) 1.
Normally, filtration of fluid out of the capillaries is slightly greater than absorption of fluid into the capillaries. The excess filtered fluid is returned to the circulation via the lymph. Lymph also returns any filtered protein to the circulation.
Lymph (function) 2. Unidirectional flow of lymph:
one-way flap valves permit interstitial to enter, but not leave, the lymph vessels. Flow through larger lymphatic vessels is also unidirectional, and is aided by one-way valves and skeletal muscle contraction.
Lymph (function) 3. Edema
occurs when the volume of interstitial fluid exceeds the capacity of the lymphatic to return it to the circulation. Can be caused by excess filtration or blocked lymphatics
Passage of substances across the capillary wall 1.
Lipid-soluble substances (o2 and CO2)
Passage of substances across the capillary wall Small water-soluble substance 2a.
cross via the water-filled clefts between the endothelial cells.
include water, Glucose, and amino acid.
Proteins molecules are too large to pass freely through the clefts.
Passage of substances across the capillary wall Small water-soluble substance 2b.
In the brain, the clefts between endothelial cells are exceptionally tight (blood-brain barrier).
Passage of substances across the capillary wall Small water-soluble substance 2c.
In the liver and intestine, the clefts are exceptionally wide and allow passage of protein. These capillaries are called sinusoids.
Passage of substances across the capillary wall Large water-soluble substances 3.
can cross by pinocytosis
Kidney
It maintains constancy of ECF volume and of osmolality by balancing intake and excretion of Na+ and water
kidney achieves
constancy of extracellular K+ concentration and of blood and cellular PH by adjusting excretion of H+ and HCO3-
kidney conserves
nutrients (e.g., glucose, amino acids) and excretes end products of metabolism (urea, uric acid)
kidney has numerous
metabolic functions (arginine formation, gluconeogenesis, peptide hydrolysis)
kidney is a source
of hormones (angiotensin II, erythropoietin, prostaglandins)
kidney Reabsorption
Whence the greater part of this ultrafiltrate is transported across the tubule wall and reenters the blood
kidney excretion
The fraction that is not reabsorbed remains in the tubules and appears in the terminal urine
kidney secretion
Some urinary solvents enter the nephron lumen from tubule cells by secretion.
Nephron
A nephron consists of a glomerulus and renal tubule.
nephron 1
The glomerulus is a glomerular capillary network, which emerges from an afferent arteriole
nephron 2
Renal tubule comprises the following segments: Proximal tubule, Loop of Henle (thin descending limb, a thin ascending and a thick ascending limb), Distal tubule, Collecting ducts
Renal vasculature step 1
Blood enters each kidney via renal artery, which branches into interlobar a., arcuate a. and cortical radial.
renal vasculature step 2
The smallest arteries subdivide into first set of arterioles, the afferent arterioles. The afferent arterioles deliver blood to the first capillary network, the glomerular capillaries.
renal vasculature step 3
Then blood leaves the glomerular capillaries, via a second set of arterioles, the efferent arterioles, which deliver blood to a second capillary network, the peritubular capillaries.
renal vasculature step 4
The peritubular capillaries surround the nephrons. Solutes and water are reabsorbed into the peritubular capillaries and a few solutes are secreted from the peritubular capillaries. Blood from the peritubular capillaries flows into small veins and then into the renal vein.
renal vasculature step 5
In the juxtamedullary nephrons, the peritubular capillaries have a specialization called the vasa recta. Vasa recta serve as osmotic exchangers for the production of concentrated urine.
Total body water (TBW) is approximately
60% of body weight
The percentage of TBW is highest
in newborns and adult males and lowest in adult females and in adults with a large amount of adipose tissue.
Plasma is
¼ of the ECF.
Interstitial fluid is
¾ of the ECF.
60-40-20 rule:
TBW is 60% of body weight, ICF is 40% of body weight, ECF is 20% of body weight
Glomerular filtration
The glomerular capillaries have large pores in their walls, and the layer of Bowman’s capsule in contact with the glomerulus has filtration slits. Water, together with dissolved solutes (but not proteins) can thus pass from the blood plasma to the inside of the capsule and the nephron tubules
glomerular filtration rate (GFR)
The volume of this filtrate produced by both kidneys per minute
Glomerular ultrafiltrate
The fluid that enters the glomerular capsule is called ultrafiltrate
Because glomerular capillaries are extremely permeable and have an extensive surface area
this modest net filtration pressure produces an extraordinarily large volume of filtrate
The GFR averages
115 ml per min in woman and 125 ml per min in men. It 180 L per day
GFR, Inulin
Measurement of GFR-clearance of inulin, Inulin is filtered, but not reabsorbed or secreted by the renal tubules. GFR= U inulin V/ P inulin. U=Urine concentration of inulin (mg/ml). P=Plasma concentration of inulin (mg/ml)
Reabsorption of glucose Step 1
Na+-glucose cotransport in the proximal tubule reabsorbs glucose from tubular fluid into the blood. There are a limited number of Na+-glucose carriers
Reabsorption of glucose step 2
At plasma glucose concentrations less than 250 mg/dl, all of the filtered glucose can be reabsorbed because plenty of carriers are available; in this range, the line for reabsorption is the same as that for filtration
Reabsorption of glucose step 3
At plasma glucose concentration greater than 350 mg/dl, the carriers are saturated. Therefore, increases in plasma concentration above350 mg/dl do not result in increased rates of reabsorption. The reabsorptive rate at which the carriers are saturated is the transport maximum ™
Excretion of glucose step 1
At plasma concentrations less than 250 mg/dl, all of the filtered glucose is reabsorbed and excretion is zero. Threshold is approximately 250mg/dl
excretion of glucose step 2
At plasma concentrations greater than 350 mg/dl, reabsorption is saturated ™. Therefore, as the plasma concentration increases, the additional filtered glucose cannot be reabsorbed and is excretes in the urine.
Na+ is filtered across the
glomerular capillaries; therefore, the Na+ in the tubular fluid of Bowman’s space equals that in plasma
Na+ is reabsorbed along the
entire nephron, and very little is excreted in urine <1% of the filtered load
Na+ reabsorption along the nephron Proximal tubule
reabsorb 2/3, or 67%, of the filtered Na+ and H2O, more than any other part of the nephron, is the site of glumerulo-tubular balance, The reabsorption of Na+ and H2O in the proximal tubule are exactly proportional
Early proximal tubule-special features
reabsorbs Na+ and H2O with HCO3-, glucose, amino acids, phosphate, and lactate
Na+ is reabsorbed by? (Early proximal tubule-special features)
cotransport with glucose, AAs, phosphate, and lactate. These cotransport processes account for the reabsorption of all of the filtered glucose and AAs
Na+ is also reabsorbed by? (Early proximal tubule-special features)
counter transport via Na+-H+ exchange, which is linked directly to the reabsorption of filtered HCO3-
Middle and late proximal tubules-special features
Filtered glucose, amino acids, and HCO3- have already been completely removed from the tubular fluid by reabsorption in the early proximal tubule
In the middle and late proximal tubules, Na+ is reabsorbed with Cl-
Thick ascending limb of the loop of Henle
reabsorbs 25% of the filtered Na+.
contains a Na+-K+-2Cl- cotransporter in the luminal membrane.
is impermeable to water. NaCl is reabsorbed without water. As a result, tubular fluid Na+ and tubular fluid osmolarity decrease to less than their concentrations in plasma This segment, therefore, is called the diluting segment
Distal tubule and collecting duct
together reabsorb 8% of the filtered Na+.
Early distal tubule-special features.
reabsorbs NaCl by a Na+-Cl- cotransporter.
is impermeable to water.
is called the cortical diluting segment
K+ Regulation A. Shifts of K+ between the ICF and ECF
Most of the body’s K+ is located in the ICF
A shift of K+ out of cells causes hyperkalemia
A shift of K+ into cells causes hypokalemia
K+ Regulation B. Renal regulation of K+ balance
K+ is filtered, reabsorbed, and secreted by the nephron
K+ balance is achieved when urinary excretion of K+ exactly equals intake of K+ in the diet
K+ excretion can vary widely from 1% to 110% of the filtered load, depending on dietary K+ intake, aldosterone levels, and acid-base status
- Glumerular capillaries
Filtration occurs freely across the glomerular capillaries
- Proximal tubule
reabsorbs 67% of the filtered K+ along with Na+ and H2O
- Thick ascending limb of the loop of henle
reabsorbs 20% of the filtered K+
Reabsorption involves the Na+-K+-2Cl- cotransporter in the luminal membrane of cells in the thick ascending limb
- Distal tubule and collecting duct
either reabsorb or secrete K+, depending on dietary K+ intake.
Secretion of K+
occurs in the principal cell
is variable and accounts for the wide range of urinary K+ excretion
depends on factors such as dietary K+, aldosterone levels, acid-base status, and urine flow rate.
Dietary K+
A diet high in K+ increases K+ secretion, and a diet low in K+ decreases K+ secretion, the alpha-intercalated cells are stimulated to reabsorb K+ by the H+, K+-ATPase
On a high-K+ diet
intracellular K+ increases so than the driving force for K+ secretion also increases
On a low-K+ diet
intracellular K+ decreases so that the driving force for K+ secretion decreases
Aldosterone
increases K+ secretion. The mechanism involves increased Na+ entry into the cells across the luminal membrane and increased pumping of Na+ out of the cells by the Na+-K+ pump.
Aldosterone Stimulation
Stimulation of the Na+-K+ pump simultaneously increases K+ uptake into the principal cells, increasing the intracellular K+ concentration and the driving force for K+ secretion. Aldosterone also increases the number of luminal membrane K+ channels
Acid-base
Effectively, H+ and K+ exchange for each other across the basolateral cell membrane
Acidosis
decreases K+ secretion. The blood contains excess H+; therefore, H+ enters the cell across the basolateral membrane and K+ leaves the cell. As a result, the intracellular K+ concentration and the driving force for K+ secretion decrease
Alkalosis
increases K+ secretion. The blood contains too little H+; therefore, H+ leaves the cell across the basolateral membrane and K+ enters the cell. As a result, the intracellular K+ concentration and driving force for K+ secretion increase.
Late distal tubule and collecting duct-special features
have two cell types, Principal cells, alpha Intercalated cells
Principal cells
reabsorb Na+ and H2O
secrete K+
Aldosterone increases Na+ reabsorption and increases K+ secretion
principal cells antidiuretic hormone
increases H2O permeability by directing the in secretion of H2O channels in the luminal membrane. In the absence of ADH, the principal cells are virtually impermeable to water
alpha Intercalated cells
secrete H+ by a H+ adenosine triphosphatase (ATP ase), which is stimulated by aldosterone
reabsorb K+ by a H+, K+-ATPase.
Urea
oFifty percent of the filtered urea is reabsorbed passively in the proximal tubule.
Rest are impermeable
ADH increases the urea permeability of the inner medullary collecting ducts
Phosphate
Eighty-five percent of the filtered phosphate is reabsorbed in the proximal tubule by Na+-phosphate cotransport. 15% of the filtered load is excreted in urine
Parathyroid hormone
inhibits phosphate reabsorption in the proximal tubule by activating adenylate cyclase, PTH causes phosphaturia and increased urinary cAMP
Calcium
Sixty percent of the plasma Ca+ is filtered across the glomerular capillaries
calcium the proximal tubule and thick ascending limb
Together, the proximal tubule and thick ascending limb reabsorb more than 90% of the filtered Ca+ by passive processes that are coupled to Na+ reabsorption
Calcium the distal tubule and collecting duct
Together, the distal tubule and collecting duct reabsorb 8% of the filtered Ca+ by an active process
calcium Parathyroid hormone (PTH)
increases Ca+ reabsorption by activating adenylate cyclase in the distal tubule
Magnesium (Mg2+)
is reabsorbed in the proximal tubule, thick ascending limb of the loop of Henle, and distal tubule
Magnesium (Mg+) thick ascending limb
In the thick ascending limb, Mg2+ and Ca+ compete for reabsorption; therefore, hypercalcemia causes an increase in Mg2+ excretion (by inhibiting Mg+ reabsorption).
ADH Mechanism of action (1)
ADH attaches to a V2 receptor and activates a cascade through a Gs protein, adenylyl cyclase, cAMP and protein kinase A to cause the insertion of aquaporin 2 into the apical membrane
ADH Mechanism of action (2)
H2O moves through aquaporin 2 in response to an osmotic gradient and thence through aquaporins 3 and 4 in the basolateral membrane
Production of concentrated urine
is also called hyperosmotic urine, in which urine osmolarity> blood osmolarity
is produced when circulating ADH levels are high (e.g., water deprivation, hemorrhage, SIADH)
Corticopapillary osmotic gradient-high ADH
is the gradient of osmolarity from the cortex (300mOsm/L to the papilla (1200mOsm/L), and is composed primarily of NaCl and urea
Corticopapillary osmotic gradient-high ADH is established
by countercurrent multiplication and urea recycling
Corticopapillary osmotic gradient-high ADH is maintained
by countercurrent exchange in the vasa recta
Proximal tubule-high ADH
The osmolarity of the glomerular filtrate is identical to that of plasma (300mOsm/L)
Two-thirds of the filtered H2O is reabsorbed isosmotically (with Na+, Cl-, HCO3-. Glucose, AAs, ) in the proximal tubule
TF/P osm= 1.0 throughout the proximal tubule because H2O is reabsorbed isosmotically with solute.
Thick ascending limb of the loop of Henle-high ADH
is called the diluting segment
reabsorbs NaCl by the Na+-K+-2Cl- cotransporter
is impermeable to H2O. Therefore, H2O is not reabsorbed with NaCl, and the tubular fluid becomes dilute
The fluid that leaves the thick ascending limb has an osmolarity of 100 mOsm/L and TF/P osm<1.0 as a result of the dilution process
Early distal tubule-high ADH
is called the cortical diluting segment
like the thick ascending limb, the early distal tubule reabsorbs NaCl but is impermeable to water. Consequently, tubular fluid is further diluted
Late distal tubule-high ADH (1)
ADH increases the H2O permeability of the principal cells of the late distal tubule
Late distal tubule-high ADH (2)
H2O is reabsorbed from the tubule until the osmolarity of distal tubular fluid equals that of the surrounding interstitial fluid in the renal cortex (300mOsm/L)
Late distal tubule-high ADH (3)
TF/Posm=1.0 at the end of the distal tubule because osmotic equilibration occurs in the presence of ADH.
Collecting ducts-High ADH (1)
as in the late distal tubule, ADH increases the H2O permeability of the principal cells of the collecting ducts
Collecting ducts-High ADH (2)
As tubular fluid flows through the collecting ducts, it passes through the corticopapillary gradient (regions of increasingly higher osmolarity), which was previously established by counter recurrent multiplication and urea recycling
Collecting ducts-High ADH (3)
H2O is reabsorbed from the collecting ducts until the osmolarity of tubular fluid equals that the surrounding interstitial fluid
Collecting ducts-High ADH (4)
The osmolarity of the final urine equals that at the bend of the loop of Henle (1200mOsm/L)
Glomerulonephritis (nephritic syndrome)
is a disorder of glomeruli. It is characterized by body tissue swelling (edema), high blood pressure, and the presence of red blood cells in the urine
Glomerulonephritis can be
Primary, affecting only the kidneys. Secondary, caused by a vast array of disorders that affect other parts of the body.
Acute Glomerulonephritis
Acute glomerulonephritis most often occurs as a complication of throat or skin infection by streptococcus, a type of bacteria.
post-streptococcal glomerulonephritis
Acute glomerulonephritis that occurs after a streptococcal infection
Infections with other types of bacteria (Glomerulonephritis causes)
such as: staphylococcus and pneumococcus, viral infections, such as chickenpox, parasitic infections, such as malaria
Noninfectious causes of acute glomerulonephritis include:
membranoproliferative glomerulonephritis, immunoglobulin A (IgA) nephropathy, systemic lupus erythematosus (lupus), Acute glomerulonephritis that develops into rapidly progressive glomerulonephritis most often results from conditions that involve an abnormal immune reaction
Chronic Glomerulonephritis
Occasionally, chronic glomerulonephritis is caused by hereditary nephritis, an inherited genetic disorder. In many people, the cause of chronic glomerulonephritis cannot be identified.
Edema (Glomerulonephritis symptoms)
Puffiness of the face, Eyelids but later is prominent in the legs
glomerulonephritis symptoms
Blood pressure, headaches, visual disturbances, coma, nausea, general feeling of illness (malaise), weakness, fatigue, fever, Loss of appetite, nausea, vomiting, abdominal pain, joint pain
glomerulonephritis treatment (diet)
Following a diet that is low in protein and sodium may be necessary until kidney function recovers. Restricting the amount of protein in the diet is modestly helpful in reducing the rate of kidney deterioration
glomerulonephritis treatment (diuretics)
Diuretics may be prescribed to help the kidneys excrete excess sodium and water
glomerulonephritis treatment (how to treat high blood pressure?)
Angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs)
glomerulonephritis treatment (antibiotics)
When a bacterial infection is suspected as the cause of acute glomerulonephritis, antibiotics
glomerulonephritis treatment (kidney failure?)
End-stage kidney failure can be treated with dialysis or a kidney transplant.
Pyelonephritis
is a bacterial infection (90% is by Escherichia Coli) of one or both kidneys. Infection can spread up the urinary tract to the kidneys, or the kidneys may become infected through bacteria in the bloodstream
Pyelonephritis symptoms
Chills, fever, back pain, nausea, and vomiting can occur. Urine and sometimes blood tests are done to diagnose pyelonephritis
Pyelonephritis treatment
Antibiotics are given to treat the infection.
Kidney stones
Stones (calculi) are hard masses that form anywhere in the urinary tract and may cause pain, bleeding, obstruction of the flow of urine, or an infection
stones causes
Stones may form because the urine becomes too saturated with salts that can form stones or because the urine lacks the normal inhibitors of stone formation
An inhibitor in stones
citrate
80% of stones are composed of? and are most common in people with
calcium, and the remainder are composed of various substances, including uric acid, cystine; hyperparathyroidism.
What kind of stones do not to be treated
Small stones that are not causing symptoms, obstruction, or an infection usually do not need to be treated
what is recommended to help stones pass
Drinking plenty of fluids has been recommended to help stones pass, but it is not clear that this approach is helpful
Drugs that help stones pass
Drugs that may help the stone pass include alpha-adrenergic blockers (such as tamsulosin)
kidney stones treatment
Potassium citrate
Calcium channel blockers (such as Verapamil)
Once a stone has passed, no other immediate treatment is needed
The pain of renal colic may be relieved with nonsteroidal anti-inflammatory drugs (NSAIDs) or opioids.
Reabsorption of filtered HCO3-
occurs primarily in the proximal tubule
Key features of reabsorption of filtered HCO3- 1a.
H+ and HCO3- are produced in the proximal tubule cells from CO2 and H2O. CO2 and H2O combine to form H2CO3 Carbonic acid, catalyzed by intracellular carbonic anhydrase
Key features of reabsorption of filtered HCO3- 1b.
H2CO3 dissociates into H+ and HCO3-. H+ is secreted into the lumen via the Na+-H+ exchange mechanism in the luminal membrane. The HCO3- is reabsorbed
Key features of reabsorption of filtered HCO3- 2.
In the lumen, the secreted H+ combines with filtered HCO3- to form H2CO3, which dissociates into CO2 and H2O, catalyzed by brush border carbonic anhydrase. CO2 and H2O diffuse into the cell to start the cycle again
Key features of reabsorption of filtered HCO3- 3.
The process results in net reabsorption of filtered HCO3-. However, it does not result in net secretion of H+.
Regulation of reabsorption of filtered HCO3- (filtered load)
Increases in the filtered load of HCO3- result in increased rates of HCO3- reabsorption. However, in the plasma HCO3- concentration becomes very high (metabolic alkalosis), the filtered load will exceed the reabsorptive capacity, and HCO3- will be excreted in the urine
Regulation of reabsorption of filtered HCO3- (Pco2 increased)
Increases in Pco2 result in increased rates of HCO3- reabsorption because the supply of intracellular H+ for secretion is increased
Regulation of reabsorption of filtered HCO3- (Pco2 decreased)
Decreases in Pco2 result in decreased rates of HCO3- reabsorption because the supply of intracellular H+ for secretion is decreased
Regulation of reabsorption of filtered HCO3- (Pco2 effects of changes)
These effects of changes in Pco2 are the physiologic basis for the renal compensation for respiratory acidosis and alkalosis
Regulation of reabsorption of filtered HCO3- (ECF volume expansion and concentration)
ECF volume expansion results in decreased HCO3- reabsorption
ECF volume concentration results in increased HCO3- reabsorption (contraction alkalosis)
Regulation of reabsorption of filtered HCO3- (Angiotensin II)
stimulates Na+-H+ exchange and thus increases HCO3- reabsorption, contributing to the contraction alkalosis that occurs secondary to ECF volume contraction.
Excretion of H+
Fixed H+ produced from the catabolism of protein and phospholipid is excreted by two mechanisms, titratable acid and NH4+
Excretion of H+ as titratable acid (H2PO4)
the amount of H+ excreted as titratable acid depends on the amount of urinary buffer present and the pK of the buffer
Excretion of H+ as titratable acid (H2PO4) Step 1
H+ and HCO3- are produced in the cell from CO2 and H2O. The H+ is secreted into the lumen by an H+-ATPase, and the HCO3- is reabsorbed into the blood (new HCO3). In the urine, the secreted H+ combines with filtered HPO4-2 to form H2PO4-, which is excreted as titratable acid
Excretion of H+ as titratable acid (H2PO4) Step 2
This process results in net secretion of H+ and net reabsorption of newly synthesized HCO3-
Excretion of H+ as titratable acid (H2PO4) Step 3
As a result of H+ secretion, the pH of urine becomes progressively lower. The minimum urinary pH is 4.4
Excretion of H+ as titratable acid (H2PO4) Step 4
The amount of H+ excreted as titratable acid is determined by the amount of urinary buffer and the pK of the buffer.
Metabolic acidosis (A)
Overproduction or ingestion of fixed acid or loss of base produces an increase In arterial (H+) (acidemia)
Metabolic acidosis (B)
HCO3- is used to buffer the extra fixed acid. As a result, the arterial (HCO3) decreases. This decrease in the primary disturbance
Metabolic acidosis (C)
Acidemia causes hyperventilation (Kussmaul breathing), which is the respiratory compensation for metabolic acidosis
Metabolic acidosis (D)
Renal correction of metabolic acidosis consists of increased excretion of the excess fixed H+ as titratable acid and NH4+, and increased reabsorption of new HCO3-, which replenishes the HCO3- used in buffering the added fixed H+.
In chorionic metabolic acidosis
an adaptive increase in NH3 ammonia synthesis aids in the excretion of excess H+.
Metabolic alkalosis (A)
Loss of fixed H+ or gain of base produces a decrease in arterial H+ (alkalemia)
Metabolic alkalosis (B)
As a result, arterial HCO3- increases. This increase is the primary disturbance.
For example, in vomiting H+ is lost from the stomach, HCO3- remains behind in the blood, and the HCO3- increases
Metabolic alkalosis (C)
Alkalemia causes hypoventilation, which is the respiratory compensation for metabolic alkalosis
Metabolic alkalosis (D)
Renal correction of metabolic alkalosis consists of increased excretion of HCO3- because the filtered load of HCO3- exceeds the ability of the renal tubule to reabsorb it
If metabolic alkalosis is accompanied by ECF volume contraction (vomiting),
the reabsorption of HCO3- increases (secondary to ECF volume contraction), worsening the metabolic alkalosis.
Motor unit recruitment
is the progressive activation of a muscle by successive recruitment of contractile units (motor units) to accomplish increasing gradations of contractile strength.
A motor unit consists of
one motor neuron and all of the muscle fibers it contracts.
When a nerve cell stimulates a muscle fiber (muscle contraction)
it sets up an impulse in the Sarcolemma that signals the Sarcoplasmic reticulum to release Calcium ions
Released Ca++ (muscle contraction)
diffuses through cytoplasm and triggers the sliding filament mechanism. Impulses further conducted by t tubules (deep invaginations of the sarcolemma)
Mechanism of contraction: Sliding filament theory
Myosin heads attach to actin in the thin filaments
Then pivot to pull thin filaments inward toward the center of the sarcomere
Contraction mechanism is activated by binding of Ca++ to the thin filaments and powered by ATP.
Types of muscle sensors
Muscle spindles (groups Ia and II afferents), Golgi tendon organ (group Ib afferents), Pacinian corpuscles (group II afferents), Free nerve endings (group III and IV afferents)
Muscle spindles (groups Ia and II afferents)
are arranged in parallel with extrafusal fibers.
Golgi tendon organ (group Ib afferents)
are arranged in series with extrafusal muscle fibers. They detect muscle tension.
Pacinian corpuscles (group II afferents)
are distributed throughout muscle. They detect vibration.
Free nerve endings (group III and IV afferents)
detect noxious stimuli
Extrafusal fibers
make up the bulk of muscle.
are innervated by alpha-motoneurons.
provide the force for muscle contraction.
Intrafusal fibers
are smaller than extrafusal muscle fibers.
are innervated by gamma-motoneurons.
are encapsulated in sheaths to form muscle spindles.
run in parallel with extrafusal fibers. But not for entire length of the muscle.
Muscle spindle
Muscle spindle reflexes oppose (correct for) increases in muscle length (stretch).
How the muscle spindle works Step 1
Sensory information about muscle length is received by group Ia (velocity) and group II (static) afferent fibers.
How the muscle spindle works Step 2
When a muscle is stretched, the muscle spindle is also stretched, stimulating group Ia and group II afferent fibers.
How the muscle spindle works Step 3
Stimulation of group Ia afferents stimulates alpha-motoneurons in the spinal cord. This stimulation in turn causes contraction and shortening of the muscle. Thus, the original stretch is opposed muscle length is maintained.
gamma-motorneurons innervate
intrafusal muscle fibers
Function of gamma-motoneurons
adjust the sensitivity of the muscle spindle so that it will respond appropriately during muscle contraction.
alpha-motorneurons and gamma-nerurons are
coactivated so that muscle spindles remain sensitive to changes in muscle length during contraction
Smooth muscle
Cells are spindle-shaped, cells are non-striated and contain no sarcomere.
Separated by endomysium.
Contain one centrally located nucleus.
Grouped into sheets in walls of hollow organs
Are in longitudinal layer or circular layer, both layers participate in contraction.
smooth muscle examples
Walls of circulatory vessels, Respiratory tubes, Digestive tubes Urinary organs, Reproductive organs, Inside the eye etc.
Smooth muscle contraction Step 1
Extracellular Ca++ diffusing into the smooth muscle cell is responsible for sustained contractions
Smooth muscle contraction Step 2
Opening of ca++ channels is graded by the amount of depolarization, the greater the depolarization, the more Ca++ will enter the cell and the stronger will be the smooth muscle contraction
Smooth muscle contraction Step 3
Ca++ combines with a protein, calmodulin, the calmodulin-Ca++ combines with and activates myosin light-chain kinase, an enzyme that catalyzes the phosphorylation of myosin light chains, then it binds to actin and thereby produce a contraction.
Smooth muscle contraction Step 4
Relaxation of the smooth muscle follows the closing of the Ca++ channels.
Duchenne
Sex-linked recessive inherited disease, males are most exclusively affected,
1/3500 boys, diagnosed between age 2-10, muscle weakens
first pelvic muscles affected, then muscles of shoulder and head, rarely live over 20 years.
Fibers lack a submembrane protein called dystrophin.
Myotonic dystrophy
is an inherited disorder in which the muscles contract but have decreasing power to relax. With this condition, the muscles also become weak and waste away
Myotonic dystrophy can cause
mental deficiency, hair loss and cataracts.
Onset of this rare disorder (myotonic dystrophy) commonly occurs during
young adulthood. However, it can occur at any age and is extremely variable in degree of severity.
The myotonic dystrophy gene
found on chromosome 19, codes for a protein kinase that is found in skeletal muscle, where it likely plays a regulatory role
