UCF Ahangari Physiology Exam #3

Function of Blood

- Transportation of respiratory gases, hormones, metabolites and nutrients

-Regulation (hormonal and temperature)

-Protection through clotting and through immune function of blood.

Hematocrit

The percentage of blood volume that consist of RBC

Males: 42-52%

Females: 37-47%

Blood

specialized connective tissue which contains cellular and liquid components.

Blood cells or formed elements

Plasma- fluid portion

Blood Plasma

straw-colored, sticky fluid portion of blood.

-90 % water

-Na, nutrients, waste, protein, enzymes, antibodies, and hormones.

Types of Plasma proteins

albumins, globulins, fibrinogen

Albumin

60-80%

-produced by liver.

- provide osmotic pressure needed to draw water from other tissues to capillaries.

- controls body fluid.

- excess leads to edema.

Globulins

-alpha, beta, gamma

-alpha and beta produced by liver, transport lipids and fat soluble vitamins, function in immunity.

- Gamma is important for treatment for hepatitis. prevent s/sx.

Fibrinogen

-important for blood clotting

-produced by liver

-fluid formed from clotted blood= serum

Blood cells (formed elements)

erythrocytes, leukocytes, platelets

Erythrocytes

-function is to transport oxygen and carbon dioxide

leukocytes

- function is to move to sites of infection through diapedesis or extravasation.

2 types of leukocytes

agranulocytes and granulocytes

Agrunolocytes

lymphocytes and monocytes

Lymphocytes

mount immune response by direct cell attack. T and B cells!

Monocytes

phagocytosis and develop into macrophages in tissues

Granulocytes

neutrophils, eosinophils, basophils

Neutrophils

phagocytize microorganisms (bacteria)

Eosinophils

turn off allergic response and kill parasites

Basophils

release histamine and other inflammatories.

RBC life span

-120 days

- aged RBC removed from blood in sinuses of spleen and are degraded.

Erythropoietin

- Hormone

- cellular O2 deficiency is initiating event in production and release of hormone erythropoietin.

- produced in glomeruli of Kidney, mainly in liver.

-Stimulates RBC production in red bone marrow

Hematopoiesis

- blood cell formation

- give rise to blood cells originating in yolk sac of human embryo then to liver of fetus. stem cells then migrate to bone marrow.

- 2 types: Myeloid and Lymphoid.

3 factors for formation of Erythrocytes

Folic acid, Iron, Vitamin B12

Polycythemia

-abnormal excess of erythrocytes

- erythrocyte disorder

s/sx: increased rbc, increased wbc, increase platelet, severe headache, hepatomegaly.

secondary: if not treated become chronic or artificial polycythemia.

Anemia

levels of hemoglobin concentrate low

-Erythrocyte disorder

Normocytic anemia

blood loss

Microcytic anemia

iron deficiency

Macrocytic anemia

Vitamin B12 or folate deficiency

sickle cell anemia

a genetic disorder that causes abnormal hemoglobin, resulting in some red blood cells assuming an abnormal sickle shape.

caused by abnormal hemoglobin S and C.

s/sx: abdominal pain, bone pain, breathlessness, fatigue, jaundice, rapid heart rate.

tx: folic acid, antibiotic and vaccines to prevent bacterial infection.

Leukemia

cancer of white blood cells

either lymphoblastic or myelogenous

s/sx: headaches, easily bleeding, swollen lymph nodes, getting many infections, weakness and weight loss.

tx: chemotherapy, interferon- alpha, radiation therapy, and stem cell transplantation.

Thrombocytopenia

abnormally low platelet concentrate

Blood vessels

Tunica Intima: inner

Tunia media: middle

Tunia externa: outside

Lumen: central blood filled space of vessel

Artery

- carry blood away from heart

-elastic arteries: largest

-Muscular arteries

arterioles: smallest, higher BP than vein.

-thicker walls because it has more elastic fibers.

- higher bp

Veins

-Carry blood to the heart

- lower BP than arteries, but higher than atrial BP

- venules: smallest. alpha 1 receptor

- Tunica externa: thickest

- have valves in limbs !!

Capillaries

- smallest blood vessel

- RBC pass through in a single file line

- site of exchange of molecules between blood and tissue fluid.

- low permeability capillaries: BBB selective, only vital substances pass, NOT barrier for O2, CO2, and anesthetics

-shows resistance from blood flow from artery.

Blood cells in embryo

gives nutrients to embryo during 1-2 months of pregnancy.

aplastic anemia

due to destruction of the bone marrow maybe be caused by chemical or radiation

Heparin

Anticoagulant

Folic acid

- important for production of red blood cells

- important for development of CNS in fetus from neural tube.

formula for blood pressure

BP= TPR x CO

resistance in capillaries

important factors that lead to hypertension

any factor that leads to vasoconstrictor, destruction or obstruction leads to hypertension.

Blood vessels from biggest to smallest

aorta -> artery -> arteriole -> capillary -> venule -> veins

AORTA largest artery in body!!

Cardiovascular system overview

1. inferior vena cava brings deoxygenated blood to right atrium

2. through the tricuspid the right ventricle fills and ejects blood to pulmonary artery through the semilunar valve or pulmonary

3. blood goes through pulmonary artery and takes blood to lungs

4. lungs release Oxygen into pulmonary capillaries then pulmonary vein

5. returns back to left atrium through pulmonary vein

5. blood from left atrium goes to left ventricle through bicuspid valve.

6. left ventricle ejects blood into aortic valve and then through there enters aorta

7. aorta releases blood out to the body.

Systemic circulation

-circulation that supplies blood to all the body except to the lungs

1. oxygen blood from lungs leaves left side of heart through aorta.

2. from aorta it is distributed into organs and tissues

deoxygenated blood enters is collected by venules then flows to veins who take it back to the heart.

pulmonary circulation

- oxygen depleted blood to lungs

1. deoxygenated blood leaves right side of heart through pulmonary artery into the lungs.

2. rbc release CO2 and pickup oxygen during respiration.

then oxygenated blood leaves lungs though pulmonary artery into the heart.

Hemodynamics

the science of the blood flow through the circulation

- components of vasculature

- velocity of blood flow

- blood flow

-resistance

-capacitance

Components of vasculature

-venules formed from merged capillaries

- veins progressively from larger veins

Velocity of blood flow

- velocity directly proportional to flow, inversely to cross sectional area at any level of cardiovascular system

blood flow

- flow is inversely proportional to resistance of blood vessels

resistance

- directly proportional to viscosity and length of blood vessel.

capacitance

- describes distenbility of blood vessels

inversely proportional to elastance and pressure, directly proportional to volume

Mean pressure

-as blood flows through systemic, pressure decreases progressively because of resistance to blood flow

aorta= 100 mm Hg

arteriole- 50 mm Hg

capillary= 20 mm Hg

Vena cava= 4 mm Hg

systolic pressure

- highest arterial pressure during cardiac cycle

measured after heart contracts, blood ejects to arterial system

diastolic pressure

-lowest arterial pressure

measured when heart relax, blood returning heart via vein.

pulse pressure

- most important determinant of pulse pressure is stroke volume.

systolic increases because of low capacitance of arteries. because diastolic stays the same, pulse pressure increases to same extent of systolic.

Venous pressure

-very low pressure

- veins have high capacitance, can hold large volume of blood at low pressure

Atrial pressure

- even lower venous pressure

- left atrial pressure is estimate by pulmonary wedge pressure.

- pulmonary capillary pressure equal to left atrial pressure

mean arterial pressure

diastolic pressure + 1/3 pulse pressure

Primary Hypertension

- unknown etiology

- environmental factor such as diet, obesity of stress can lead to an increase of total peripheral vascular resistance by inducing vasoconstriction.

BP= CO x TPR

- sympathetic nervous system and renin angiotensin- aldosteron system have received the most attention to pathophysiology of Increase BP, both increase of CO + TPR

Sodium= abnormal Na crosses cell wall, increases intracell Na. cell more sensitive to sympathetic stimulation, Calcium follows Na, accumulate Ca responsible for sensitivity.

- deficiency of vasodilator substance= prostaglandins and bradykinin.

secondary hypertension

- high BP caused by conditions that affect your kidneys, arteries, heart, endocrine, pregnancy.

- things like disorders of adrenal gland, cushing syndrome, hyperaldosteronism, preeclampsia, pheochromocytoma, kidney disease, drugs, thyroid and parathyroid problems, etc.

s/sx of hypertension

- usually asymptomatic

- headache, fatigue, shortness of breath, dizziness, convulsions, changes in vision, nausea, vomiting, anxiety, increased sweating, nose bleeds, flushed face, etc.

Drugs to treat hypertension

Angiotensin - converting enzyme inhibitors:

Block formation of Angiotensin II, preventing

vasoconstriction. = capopril, ramipril

angiotensin II receptor blocker= Valsartan

Diuretic thiazide= Hydrochlorothiazide

calcium channel blocker= Felopine, Benidipine

Beta adrenergic blocker- Propanolol

ECG

electrocardiogram

P wave

- represents the wave of depolarization that spread from SA node through atria.

- usually 0.08-0.1 secs

- represents only atrial depolarization. NOT repolarization.

PR interval

Period of time from onset P wave to beginning of QRS complex.

- usually 0.12- 0.20 secs

- represents time between atrial depolarization and onset ventricular depolarization

PR interval > 0.2 sec= AV conduction block!!

QRS complex

- represents ventricular depolarization

- 0.06-0.1 secs, occurs fast!

- if prolonged >0.1 secs= conduction impaired ventricles

ectopic foci/pacemakers

cardiac tissue outside the normal cardiac conduction pathway that generates action potentials= results in impulse to slower pathways.

ST segment

-end of S wave to beginning of T wave

- ventricles complete depolarization

- important to diagnose ventricle ischemia and hypoxia

- ST can become depressed or elevated

T wave

- represents last remnant ventricular repolarization, longer than depolarization

- sometimes U wave follows T wave

U wave

- represents last remnant of repolarization

- inverted or prominent U wave= condition affecting repolarization.

QT interval

- beginning of Q wave and end of T wave presents ventricular depolarization and repolarization.

- rough estimate of average ventricular potential time

-0.2- 0.4 secs

- high HR, shorten ventricular AP, decrease QT

- Important for diagnostic of tacharythmias

Cardiac action potential ( atria, ventricle, purkinje system)

- resting stable membrane. 90 mV, K equilibrium potenital

- long duration

Phase 0- upstroke of AP, caused by increase of Na conductance, results in increase inward Na. peak of AP, Membrane Na equilibrium.

Phase 1- brief period initial repolarization, caused by outward current, movement for K ions in and out of cell.

Phase 2- Plateu of AP, cause by increase in Ca, Increase in K conductance outward and inward currents are equal which need to Plataue.

Phase 3- repolarization, Ca decreases, K increases

Phase 4- resting membrane potential, K equilibrium potential

Cardiac action potential( SA node)

-pacemaker of heart, unstable resting potential

Phase 0- upstroke of AP, increase Ca, ionic phase of SA node is different to Purkinje system.

Phase 3- repolarization due to increase of K

Phase 4- slow depolarization, pacemaker activity of SA node increase Na, results in inward Na.

cardiac action potential (AV node)

- upstroke of AP in AV node= result of inward Ca current

Conduction velocity

- time required for excitation to spread through cardiac tissue

- depends on size of upstroke AP, the larger inward, increases conduction velocity.

- fastest in the purkinje system

- slowest in AV node

Excitability

- ability of cardiac cells to initiate AP response inward, depolarization

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

- changes over course of AP, changes in excitability are described by refractory periods

Absolute refractory period

- NO AP can be initiated

Effective refractory period

- slightly longer

- conducted AP cannot be generated

Relative refractory period

- AP can be elicit but more than usual inward current

Autonomic affects on the Heart (Chronotropic)

- produce change in heart rate

Negative: decrease heart rate by decreasing the firing rate of SA node

Positive: increases heart rate by increasing the firing rate of SA node.

Autonomic affects on the Heart (Dromotropic)

-produce change in conduction velocity, in AV node

Negative: decreases conduction velocity through AV node, slows conduction action potential from atria to ventricles, increase PR interval

Positive: opposite of negative effect

Autonomic affects on the Heart (Inotropic)

Negative: decreases force of contraction

Positive: increases force of contraction

Sympathetic effect on the coronary arteries

+ effects, vasodilation

Parasympathetic effect on the coronary arteries

- effects, vasoconstriction

Arrhythmia

- result in abnormalities in impulse formation or in impulse conduction, disturbance in formation of impulse lead to change in sinus rhythm.

Sinus Tachycardia

-sinus frequency rises above 100 bpm

- normal during exercise, psychic excitation, fever

Sinus Bradycardia

-below 50-60 bpm

-normal while sleeping

Supra-ventricular arrhythmia

- due to atrial or nodal extrastyole

1. abnormal or ectopic impulse may arise in atria, AV or ventricle

2. impulse from atrial or nodal ectopic foci transmitted to ventricle

3. thrown out of sinus rhythm

P WAVE IS DEFORMED, QRS COMPLEX IS NORMAL!!

Ventricular extrasystole

-Common mechanism: automaticity, reentry

-Automaticity: the development of new site of depolarization in non-nodal ventricular tissue leads to VPC

-Reentry: reentry typically occurs when slow conducting tissue is present adjacent to normal tissue

- Possible causes: ischemia, Digoxin, Myocarditis, cardiomyopathy, Hypoxia, Mitral valve prolapse, smoking, alcohol, cocaine, caffeine, Mg, Ca excess

S/Sx: chest pain, faint feeling, fatigue, hyperventilation

Tx: restoring balance of Mg, K, Ca in body!!!

Pharmacological: sodium channel blocker like lidocaine, Phenytoin

Beta blocker like catecholamine, Atenolol, Propranolol, Metoprolol

K blocker like Sotalol

Ca blocker= Verapamil + Dilimiazem

Hypercalcemia leads to?

Arrhythmias!!

Atrial tachycardia

-rhythm disturbance in atria 100-250 bpm

Ventricular tachycardia

-rapid sequence of ectopic ventricular impulse

120-250 bpm

-can lead to cardiac arrest

AV node block

PR interval normally: 0.12-0.20 secs

- damage to AV shows in PR interval

1st degree AV node block

PR interval exceeds 0.2 secs

2nd degree AV node block

- AV damaged severely one out of 2,3,4 waves pass through, ecg P waves not associated with QRS

3rd degree AV node block

- none atrial waves pass through AV node

Complete disconnection between atria and ventricle

Excitation- Contraction coupling

1. AP spreads from cell membrane into T Tubules

2. during plateau of AP, Ca conductance increases, Ca enters cell from extracell fluid

3. Ca entry triggers release of Ca from SR

4. as a result Ca release, Intracell Ca increases

5. Ca bind with troponin C, tropomyosin moved out way so Myosin can attach to Actin

6. they bind, slide by each other, myocardial cell contract

7. relaxation when Ca reaccumulates by SR by active Ca ATPase pump.

Contractibility

- the intrinsic ability of cardiac muscle to develop force at given muscle length inotropism

- related to intra Ca concentration

Positive Inotropic ( contractibility)

produces increases in contractibility

Negative inotropic ( contractibility)

produces decreases in contractibility