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1. How each of the Autonomic Nervous Systems effect MAP

1.1. Sympathetic

1.1.1. Increases HR:

1.1.2. Increases force of contraction

1.1.3. Increases EDV: by squeezing viens to get more blood into the heart before the ventricular contraction

1.2. Parasympathetic

1.2.1. decreases HR: Bracycardia

2. when a build up of metabolites causes vasodilation to occur so that blood will flow more abudnantly to an area


3.1. Opening of valves:

3.1.1. AV valves: Opening When AV valves open, it is because atrial pressure is exceeding ventricular pressure. Thus the blood flows into the ventrial Closing When AV Valves close it is because ventricular pressure is exceeding atrial pressure

3.1.2. Semi lunar valves Opening: When the ventricles contract the pressure exceeds atrial pressure, causing the semi-lunar valve to open (the AV valves are shut) Closing: As the ventricles relax, aortic and pulmonary pressure exceed ventricular pressure and the semi-lunar valves snap shut.

4. Order of events in the Caridac Cycle: Blood flow and Heart Anatomy

4.1. 1: Deoxygenated blood enters the RA through the vena cava

4.2. 2: Blood goes down to the RV through the tricuspid vavle

4.3. 3: Blood gets pushed through the semi-lunar valve into the pulmonary artery

4.4. 4: Blood goes to the lungs

4.5. 5: From the lungs, oxygenated blood comes back to the heart through the pulmonary vien

4.6. From the pulmonary vein, blood flows into the LA, down the mitral valve and into the LV.

4.7. The strong LV pumps blood into the aorta (through the aortic valve) and to the rest of the body

5. Polarization

5.1. Depolarization

5.1.1. the excitatory response caused by action potentials

5.2. Repolarization

5.2.1. the inhibitory response which causes action potentials to relax

6. Has two types of cells

6.1. Contractile cells

6.1.1. muscle cells -- they do the mechanical work

6.2. Electrical Activity goes praidly to AV node via internodal parth way

6.3. Autorythmic (pacemaker) cells

6.3.1. The Cardiac Conduction Cycle Sympathetic Stimulation SA Node AV Node SA node Depolarizes Depolarization moves through ventricular conducting system to the apex of the heart Depolarization wave spreads upward from the apex

6.3.2. they are capable of self-generating electrical activity Just like skeletal muscle: Excitation-Contraction coupling: there must be an electrical signal to increase intracellular calcium and start contraction The Nervous Systems Role in generating electricity for the heart Parasympathetic Stimulation SA Node AV Node

7. Cardiac Cells

7.1. dependent upon Aerobic Metabolism

7.1.1. From the krebs cycle

7.2. Hypertrophy in response to increased demand of excersice, and high blood preasure

7.2.1. Good growth during exsercise

7.2.2. Bad growth high blood preasure

8. Excitation - Contraction Coupling

8.1. Much like skeletal muscle (t-tubules, troponin, and tropomyosin)

8.2. External Ca++ joins with Ca++ from the sarcoplasmic reticulum to cause overall increase in intracellular Ca++ (to make a larger contraction?)

8.3. ECG:

8.3.1. P Wave: Spread electrical activity, SA node is depolarizing and causing the atria to contract, (ventricles are relaxing

8.3.2. PQ Segment: Corresponds to the plateu phase of atrial contraction potential. Impulse travels to the AV node. Isovolumetric contraction is occuring here Isovolumetric contraction refers to early ventricular systole and occurs when the AV valve is closed and the pressure is building up the ventricals Pressure building up in the ventricles is the reason why it occurs

8.3.3. QRS Complex: Represents the spread of depolarization through the A-V bundle, (of His) bundle branches, Purkinje fibers and ventricular musculature

8.3.4. S-T segment: Ventricles are completely depolarized, this is the plataeu phase of ventricular action potentials its position and shape are important in diognosis:

8.3.5. T Wave: Represents repolarization of the ventricular muscle Isovolumetric relaxation:

8.3.6. T-P Segment: The time from the end of the T wave to the beginning of the P wave of the next cycle. This represents the diastolic pause when the entire heart is depolarized. During most of this segment the heart

8.4. There is always a contraction proceeding that area's depolarization

9. The Cardiac Cycle

9.1. One complete cycle cycle consists of atrial systole, atrial diastole, ventricular stosyole and ventricular diastole

9.1.1. Diastole- relaxation

9.1.2. Systole-contraction

9.2. Identical events are happening simultaneously on the right side of the heart. The only difference is that the pressures generated on the right side are much lower than those generated on the left side

9.3. Important terms

9.3.1. End Diastolic Volume (EDV) Volume at the end of filling (?) the amount of blood in the ventricles at the end of atrial systole just prior to ventricular contraction usually refers to the ventricles

9.3.2. End Systolic Volume (ESV) any point when the heart is contracting usaually we just mean the ventricles

9.3.3. Stroke Volume How much blood is being pumped per beat

9.3.4. Diastole relaxation

9.3.5. Systole contraction

9.4. The Order of Events: Deplarization

9.5. 1) Blood enters the atria (atrial filling) and may continue on into the ventricles

9.6. 2) Atria contracts to force last bit of blood into ventricles (ventricular filling or diastole)

9.6.1. AV- Valve closes, as atrial pressure is now lower than ventricular pressure

9.7. 3) Ventricles undergo isovolumetric contraction

9.7.1. Isovolumetric Contraction is the initialinitial phase of ventricular contraction in which tension and pressure in the ventricle increase, but no blood is pumped or ejected from the heart

9.8. 4) When ventricular pressure exceeds aortic/pumonary atery pressure, semilunar valves open and ejection occurs.

9.8.1. Semi-lunar valve; both the tricuspid and the mitral valves; the valves that allow blood to

9.9. 5) Semilunar vavles close (dub) when ventricular pressure falls below arterial pressure and ventricles undergo isovolumetric relaxation

9.10. 6. When ventricular pressure falls below atrial pressure and blood that has been accumulating in atria pours into ventricles

9.11. Ventricular Filling

9.11.1. 70% of the blood returning to the heart flows directly through the atrium into the ventricle. Atrial contraction ejects the rest. It is significant that most of the ventricular filling occurs during early diastole.During times of rapid heart rate, the duration of diastole is greatly reduced (more so than systole) which decreases the time for ventricular filling. Since most ventricular filling is occurring early in the diastole period, it is not seriously impaired. At heart rates greater than 200 bpm diastole is too short to allow adequate ventricle filling and SV falls.

9.12. Representented

10. Blood Preassure and Blood Vessels

10.1. Who gets blood?

10.1.1. Determined By 1) Metabolic need 2) Organ function (ie what is the priority at the moment) The brain ALWAYS receives a constant supply of blood.

10.1.2. Caused By: metabolites acting as vasodolaters Technical terms: Active Hypernea: Reactive Hypernea:

10.2. Blood Vessels

10.2.1. Arteries: take blood away from the heart conducting vessels that are PRESSURE (lots of elastic thick walls) Help blood get pumped around the heart they have an elastic nature to help push blood around Aretolies very small artery that leads to a resistance capillary, ALSO CALLED A RESISTANCE VESSEL Sympathetic Nervous System

10.2.2. Capillaries Exchange vessels: walls consist of a single layer of endothelium, smallest of blood vessels where physical exchange occurs between the blood and tissue cells surrounded by interstitial fluid Will leak excessive fluid if blood pressure is too high

10.2.3. Veins takes blood too the heart capacitance vessles (has a ability to storre electrical charge {probably when blood pressure gets to low]) must have vavles because blood pressure is low, so there can't be any backflow

10.3. Liver makes plasma protiens

10.4. MAP = CO X TPR

10.4.1. MAP = Mean Arterial Preassure ( that is average pressure measured in the areterials) CO=Cardiac output HRxSV TPR = Resistence

10.5. Blood Pressure Regulation

10.5.1. SHOCK inadequate delivery of blood to tissues HYPOVOLEMIC SHOCK (aka cold shock) inadequate amount of blood (Vasoconstriction) Hemorrhagic shock Traumatic shock Burn Shock CARDIOGENIC OR CIRCULATORY SHOCK Myocardial Infarction: Congestive Heart Failure Arrhythmias:

10.5.2. When MAP drops, the body will quickly attempt to correct the problem MAP is sensed by baroreceptors How they work to attempt the problem - Effectors:

10.6. DISTRIBUTIVE SHOCK( aka warm shock) blood volume is normal, but the blood is in the wrong place and is not being delivered to vital tissues (Vasodilation)

10.6.1. Fainting: nerogenic vasodilation of arterioles

10.6.2. Anaphylaxis: systemic (body wide) allergic reaction causing widespread histamine like repsonse

10.6.3. Sepsis reaction to toxins in blood; causes widespread vasodilation of arterioles "Tachycardia"

11. Capillaries

12. Pulmonary Gas Exchange and Transport: Its purpose is to purify O2 by exchanging the metabolic waste of the Krebs Cycle: CO2; and receive O2 to support the Kreb's cycle

12.1. Gas Transport: IMPORTANT

12.1.1. alveoli and capillaries exchange and blood at alveolar capillary interface because those interfaces are so thin Hemoglobin = boat Plasma = river River bed = Capillaries 1 Hemoglobin has four seats for

12.1.2. Carbon Monoxide: attaches onto the hemoglobin

12.2. Atmospheric Pressure: at sea level is 760

12.2.1. 79% Nitrogen

12.2.2. 21% Oxygen PO2= 160 mm Hg @sea level 21%/760 PO2 = 100 in alveoli PO2 = 120 in exhaled airi Question: Why is there more PO2 in expired air than in the alveoli? Initially, the air we intake does all reach the alveoli. This O2 becomes a part of what you expire when you exhale

12.2.3. >1% CO2 PCO2 = > 1%

12.3. Chemoreceptors

12.3.1. Ventilation rate and depth may be changing depending on the need to regulate thel blood levels of O2 and CO2 and pH (which is tightly controlled) pH levels are allowed to vary between

12.3.2. Central chemoreceptors very sensitive to changes in PCO2 but not to other inputs

12.3.3. Periphreal chemoreceptors capable of responding to arterial blood loevels of PO2, PCO2, and pH but are not as senitive Primarily respond to decreasing arterial PO2 but it must fall below 60 mm HG to iniate a good response

12.3.4. Only sensing plasma not what's on hemoglobin 98% of plasma is on hemoglobin which means, that chemoreceptors are unable to detect Carbon Mondoxide since those molecules take the four seats on hemoglobin

13. The Renal System

13.1. Kidney Functions:

13.1.1. Fluid homeostatsis: removes waste products from the body while matinaing a balance of substances for vital body function Electrolyte regulation: NA+, K+, H+, Ca2+, Mg3+, C1-, HSO4-, PO3 pH levels (have chemoreceptors) MAP regulation of salt and chloride ions Osmolarity (Angiotensiogen II) Waste Products (urea) Receptors involved in fluid homeostasis osmoreceptors primary baroreceptors Renal baroreceptors Hormones involved with fluid homeostasis ADH: Angiotensin II Aldosterone: Atrial Natiuretic Peptide (Factor): released from the atria when they are stretched due to increased pressure (increased blood volume). Increases sodium and water excretion, thus reducing blood colume in isosomtic fashion (the opposite of aldosterone) Peptide

13.1.2. Blood pressure regulation NA+ balance (determines blood volume) Production of Angiotensin II

13.1.3. Secretion of EPO stimulates formation of RBS in response to decrease of MAP decrease in PO2 Two ways epo is released decrease MAP decrease in PO2

13.1.4. Glyconeogenisis synthesis of glucose from amino acids made from kidenys liver

13.2. Anatomy

13.2.1. Features of a nephron Afferent/efferent arterolies Bowman's capsule Proximal convoluted tubule Loop of Henle Distal convoluted tubule (DCT) Collecting duct Peritubular capillaries

13.3. Renal Function:

13.3.1. Nephron Peritublular capillaries

14. Digestive System

14.1. Contribution of other body systems to the digestive system

14.2. The function of the digestive system is to break down the foods you eat, release their nutrients, and absorb those nutrients into the body.

14.3. Digestive Processes

14.3.1. Mastication: Mastication or chewing is the process by which food is crushed and ground by teeth. It is the first step of digestion, and it increases the surface area of foods to allow a more efficient break down by enzymes.

14.3.2. Segmentation Segmentation involves contractions of the circular muscles in the digestive tract,

14.3.3. Peristasis hte involuntary constriction and relaxation of the muscles of the intestine or another canal, creating wavelike movements that push the contents of the canal forward.

14.3.4. Digestion actual breakdown of foodstuffs. Digestion can be further categorized as mechanical or chemical digestion There are three primary categories of nutrients

14.3.5. absorbtion movement of small "absorbable" molecules from the lumen of the digestive tract to the blood or lymph

14.4. Digestive System Organs

14.4.1. Alimentary Organs "to nourish" comprised of

14.4.2. Functions of organ system

14.4.3. Accessory Structures Mechanical digestion mouth teeth tounge Salivary gland begins chemical digestion

14.5. Anatomy

14.5.1. Mouth/Pharynx/Esophagus Saliva: (a) chemical digestion of carbohydrates

14.5.2. Stomach Major function: storage of ingested food (while awaiting digestion) Chemical digestion: HCI (parirtal cells) Pepsinogen (chief cells) Mechanical digestion = strong peristlatic contractions

14.5.3. Small Intestine; Major function: absorption of nutrients Segments duodenum jejunum Ileum villi and microbilli greatly increase the surface are available for absorbtion

14.5.4. Large instestine or colon: Major function: absorbtion of water and lemination of solid feces segments caecum