UCF Physiology Exam 3

hematocrit

percentage of blood volume that consists of red blood cells

- males: 42-45%

- females: 37-47%

functions of blood

1. transportation

- carries respiratory gases, metabolites

- nutrients

2. regulation (hormonal, temperature)

3. protection

- clotting, circulatory system protects against blood loss from injury and foreign microbes or toxins introduced into the body

- immune, immune function oft he blood is performed by leukocytes that protect against many diseases

albumin

plasma protein produced by the liver and provide the osmotic pressure needed to draw water from the surrounding tissue fluid into the capillaries (60-80%)

globulins

plasma proteins in which the alpha and beta globulins are produced by the liver and function in transporting lipids and fat-soluble vitamins and function in immunity

fibrinogen

plasma protein that is an important clotting factor produced by the liver. the fluid from clotted blood, called serum

function of erythrocytes (RBC)

transport oxygen and carbon dioxide

function of leukocytes (WBC)

defense and immunity

lymphocytes

- most important cells of the immune system, their nucleus stains dark purple

- effective in fighting infective organisms, act against a specific foreign molecule (antigen)

T cells

class of lymphocyte that attacks foreign cells directly

B cells

class of lymphocytes that multiply to become plasma cells, secrete antibodies

monocytes

- largest leukocytes

- phagocytic cells

- nucleus: kidney shaped

- transform into macrophages

RBC life span

120 days

hematopoiesis

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

erythropiesis

refers to the formation of erythrocytes, and leukopoiesis to the formation of leukocytes

three factors of formation of erythrocyte

supply of iron, vitamin B12, folic acid

polycythemia

abnormal excess of erythrocytes

anemia

erythrocyte levels or hemoglobin concentrations are low

symptoms of anemia

- attacks of abdominal pain

- bone pain

- breathlessness

- delayed growth and puberty

- fatigue

- fever

- jaundice

- paleness

- rapid heart rate

- ulcers on the lower leg

treatment for anemia

- folic acid supplements

- antibiotics and vaccines are given to prevent bacterial infections

sickle cell disease

inherited condition, defective hemoglobin molecule, erythrocytes distort into a sickle shape

leukemia

- form of cancer

- classified as lymphoblastic or myeloblastic

- starts in the bone marrow, the soft tissue inside most bones

- bone marrow is where blood cells are made

- bone marrow starts to make a lot of abnormal WBCs, called leukemia cells

- they don't do the work of normal WBCs, they grow faster than normal cells, and they don't stop growing when they should

symptoms of leukemia

- 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

treatment for leukemia

1. chemotherapy to kill leukemia cells using strong anti-cancer drugs

2. interferon-alpha (INFa) therapy to slow the reproduction of leukemia cells and promote the immune system's anti-leukemia activity

3. radiation therapy to kill cancer cells by exposure to high-energy radiation

4. stem cell transplantation (SCT) to enable treatment with high doses of chemotherapy to radiation therapy

arteries

carry blood away from the heart

elastic arteries

- the largest arteries

- high elastin diameters range from 2.5 cm to 1 cm (aorta and its major branches)

- also called conducting arteries

arterioles

smallest arteries

three types of arteries

elastic, muscular, arterioles

veins

- carry blood toward the heart

- conduct blood from capillaries toward the heart

- blood pressure is much lower than in arteries

- tunica externa is the thickest tunic

- some have valves

- skeletal muscle pump

skeletal muscle pump

muscle press the veins and push the blood toward the heart

venules

smallest veins

postcapillary venules

smallest venules

capillaries

smallest blood vessels, diameter from 8-10µm, RBCs 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

weak, leaky capillaries found in the spleen, liver

circulation through the heart

- after flowing through the body, blood enters the heart at the right atrium. from the right atrium, it passes through the right atrioventricular valve and into the right ventricle. 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

- after passing through the lungs, removing CO2 and picking up oxygen (O2), the blood returns through the pulmonary vein to the left atrium. from here the blood enters the left ventricle through the left atrioventricular valve

- when the left ventricle contracts, blood is ejected through the aortic valve into the aorta and out to the body

systemic circulation

- 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

- oxygenated blood from the lungs leaves the left heart through the aorta, from where it is distributed 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. 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. the blood is then re-oxygenated through the pulmonary circulation before returning again to the systemic circulation

pulmonary circulation

- 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

- 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

- the oxygenated blood then leaves the lungs through the pulmonary veins, which return it to the left heart, completing the pulmonary cycle

- 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

- thick-walled, with extensive elastic tissue and smooth muscle

- under high pressure

- blood volume contained in the arteries is called the stressed volume

hemodynamics: arterioles

- smallest branches of the arteries

- the site of highest resistance in the cardiovascular system

- have a smooth muscle wall that is extensively innervated by autonomic nerve fibers

- arteriolar resistance is regulated by the autonomic nervous system (ANS)

- alpha-1 adrenergic receptors are found on the arterioles of the skin, splanchnic, and renal circulations

- beta-2 adrenergic receptors are found on arterioles of skeletal muscle

hemodynamics: capillaries

- consist of a single layer of endothelial cells surrounded by basal lamina

- thin-walled

- the site of exchange of nutrients, water and gases

hemodynamics: venules

formed from merged capillaries

hemodynamics: veins

- progressively merge to form larger veins. the largest vein, the vena cava, returns blood to the heart

- thin-walled

- under low pressure

- contain the highest proportion of the blood in the cardiovascular system

- the blood volume contained in the veins is called the unstressed volume

- have alpha-1 adrenergic receptors

velocity of blood flow

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

- thus, blood flows from high pressure to low pressure

- blood flow is inversely proportional to the resistance of the blood vessels

resistance

- resistance is directly proportional to the viscosity of the blood. for example, increasing viscosity by increasing hematocrit will increase - resistance and decrease blood flow

resistance is directly proportional to the length of the vessel

capacitance

- describes the distensibility of blood vessels

inversely related to elastance.

- the greater the amount of elastic tissue in a blood vessel, the higher the elastance, and the lower the compliance

- directly proportional to volume and inversely proportional to pressure

- describes how volume changes in response to a change in pressure

- 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 for aorta

100 mm Hg

mean pressure for arterioles

50 mm Hg

mean pressure for capillaries

20 mm Hg

mean pressure for vena cava

4 mm Hg

systolic pressure

- highest arterial pressure during a cardiac cycle

- measured after the heart contracts (systole) and blood is ejected into the arterial system

diastolic pressure

- lowest arterial pressure during a cardiac cycle

- measured when the heart relaxed (diastole) and blood is returning to the heart via the veins

pulse pressure

- difference between the systolic and diastolic pressures

- the most important determinant of pulse pressure is 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

venous pressure

- very low

- veins have a high capacitance and therefore, can hold large volumes of blood at low pressure

atrial pressure

- even lower than venous pressure

- left atrial 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

primary hypertension

- environmental factors (dietary Na+, obesity, and stress), whatever the responsible pathogenic mechanisms, they must lead either to increased total peripheral vascular resistance (TPR) by inducing vasoconstriction or to increased cardiac output (CO), or both. because BP = CO x TPR (resistance)

- sympathetic nervous system and renin-angiotensin-aldosteron system have received the most attention for the pathophysiology of hypertension, both can increase CO and TPR

- Na+: 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+. increased intracellular Na+, which makes the cell more sensitive to sympathetic stimulation. 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; can also occur during pregnancy

1. disorders of the adrenal gland

2. Cushing's syndrome (a condition caused by an overproduction of cortisol)

3. hyperaldosteronism (too much aldosterone)

4. pheochromocytoma (a rare tumor that causes over secretion of hormones like adrenaline and NA)

5. kidney disease: polycystic kidney disease, kidney tumor, kidney failure, or a narrow or blocked main artery supplying the kidney

6. drugs: such as corticosteroids (anti-inflammatory drugs like prednisone), leads to increased systolic, diastolic pressures and increases arterial resistance

7. nonsteroidal anti-inflammatory drugs (Motrin, Aleve), weight loss drugs (such as Meridia). salt and water retention, sympathetic activity, loss of renal vasodilation

8. coarctation of the aorta, a birth defect in which the aorta is narrowed

9. pre-eclampsia, a condition related to pregnancy, endothelial dysfunction in the maternal blood vessels

10. thyroid and parathyroid problems

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 palpatations

- general feeling of unwellness

- increased urination frequency

- flushed face

- pale skin

treatment of hypertension

- 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, Propanolol

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

- represents atrial depolarization

- 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 is termed the PR interval, which normally ranges from 0.12 to 0.20 seconds in duration. this interval represents the time between the onset of atrial depolarization and the onset of ventricular depolarization

- if the PR interval is > 0.2 seconds, 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 (> 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

- segment from the end of the S wave to the beginning of the T wave

- represents the period when the ventricles completely are depolarized

- important in the diagnosis of 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)

- sometimes a small positive U wave may be seen following the T wave. this wave represents the last remnants of ventricular repolarization. inverted or prominent U waves indicates undelrying pathology or conditions affecting repolarization

QT interval

- interval from the beginning of the Q wave to the end of the T wave

- represents the time for both ventricular depolarization and repolarization to occur, and therefore roughly estimates the duration of an average ventricular action potential. this 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 QT interval. because prolonged QT intervals can be diagnostic for susceptibility to certain types of tachyarrhythmias

- represents the entire period of depolarization and repolarization of the ventricles

cardiac action potentials: phase 0 ventricles, atria and Purkinje system

- the upstroke of the action potential

- caused by a transient increase in Na+ conductance. this increases 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 potentials: phase 1 ventricles, atria and Purkinje system

- 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 potentials: phase 2 ventricles, atria and Purkinje system

- plateau of the action potential

- 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 potentials: phase 3 ventricles, atria and Purkinje system

- repolarization

- during phase 3, Ca2+ conductance decreases, and K+ conductance increase and therefore predominates

- the high K+ conductance results in a large outward K+ current (lk) which hyperpolarizes the membrane back toward the K+ equilibrium potential

cardiac action potentials: phase 4 ventricles, atria and Purkinje system

- resting membrane potential

- a period during which inward and outward current (lk1) are equal and the membrane potential approaches the K = equilibrium potential

cardiac action potentials: phase 0 sinoatrial node

- upstroke of the action potential

- 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)

cardiac action potentials: phase 3 sinoatrial node

- repolarization

- caused by an increase in K+ conductance. this increase results in an outward K+ current that causes repolarization of the membrane potential

cardiac action potentials: phase 4 sinoatrial node

- slow depolarization

- accounts for the pacemaker activity of the SA node (automatically)

- caused by an increase in Na+ conductance, which results in an inward Na+ current called lf (slow depolarization, produced by the opening of Na+ channels and an inward Na+ current called lf)

conduction velocity

- reflects the time required for excitation to spread throughout cardiac tissue

- 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

- fastest in the Purkinje system

- 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

- the ability of cardiac cells to initiate action potentials in response to inward, depolarizing current

- reflects the recovery of channels that carry the inward currents for the upstroke of the action potential

- 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 -70 mV. during RRP it is possible to generate a second action potential (which is an abnormal configuration and shortened plateau phase)

chronotropic effects on the heart

- produce changes in heart rate

- negative chronotropic effect decreases heart rate by decreasing the firing rate of the SA node

- positive chronotropic effect increases heart rate by increasing the firing rate of the SA node

dromotropic effects on heart

- produce change sin conduction velocity, primarily int he 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

- 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

inotropic effects on heart

negative inotropic decreases force of contraction, a positive inotropic effect increases force of contraction

arrhythmias

results from abnormalities in impulse formation or in impulse conduction, disturbances in the formation of impulses lead to change in the sinus rhythm

supraventricular arrhythmia

- abnormal or ectopic (heterotopic) impulses may arise in the atria (atrial), in the AV node (nodal) or in the ventricle (entricular). 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

ventricules premature complexes (VPCs) are ectopic impulses originating from an area distal to the His Purkinje system. VPCs are the most common ventricular arrhythmia. in this case the QRS complex of the ES is deformed

two mechanisms for VPCs

automaticity and re-entry

automaticity

development of a new site of depolarization in non-nodal ventricular tissue, which can lead to a VPC. increased automaticity could be due to electrolyte abnormalities or ischemic myocardium

re-entry circuit

typically occurs when slow-conducting tissue (eg, infarcted myocardium) is present adjacent to normal tissue. the slow-conducting tissue could be due to damaged myocardium, as in the case of a healed MI

causes of ventricular extrasystole

- 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

symptoms of ventricular extrasystole

- chest pain

- faint feeling

- fatigue

- hyperventilation (after exercise)

- frequent episodes of continuous 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 for ventricular extrasystole

- restoring the balance of magnesium, calcium and potassium within the body

- pharmacological agents

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. this condition is AV node block

first degree AV node block

PR interval exceeds 0.20 seconds

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

steps in excitation-contraction coupling

1. the action potential (AP) spreads from the cell membrane into the T tubules

2. during the plateau of AP, Ca2+ conductance is increased and Ca2+ enters the cell from extracellular fluid (inward Ca2+ current)

3. this Ca2+ entry triggers the release of even Ca2+ from the SR (Ca2+ induced Ca2+ release)

4. as a result of this Ca2+ release, intracellular (Ca2+) increases

5. Ca2+ binds to troponin C, and tropomyosin is moved out of the way, removing the inhibition of action and myosin binding

6. actin and myosin binds, the thick and thin filaments slide past each other, and the myocardial cell contracts

7. relaxation occurs when Ca2+ is reaccumulated by the SR by an active Ca2+-ATPase pump

contractility

- intrinsic ability of the cardiac muscle to develop force at a given muscle length, it is also called inotropism

- related to intracellular Ca2+ concentration

- can be estimated by the ejection fraction (stroke volume/end-diastolic volume), which is normally 0.55 (55%)

positive; contractility

_______ inotropic agents produce an increase in __________

negative; contractility

_______ inotropic agents produce an decrease in _______

factors that increase contractility

- increased heart rate

- sympathetic stimulation

- cardiac glycoides