Biology 141 Physiology Exam 3 - Cardio Vascular And Circulatory System

Front 1

Electrocardiogram (ECG)

Back 1

Measures the electrical activity of the heart

Front 2

Automaticity

Back 2

The ability of each heart cell to reach action potential without an external stimulation. Independent of each other.

Front 3

Pacemaker Cells

Back 3

Establish heart rate. They are primary because they are able to reach threshold faster than other cells. Initiates chain reaction, other cells follow.

Front 4

Sinoatrial Node (SA)

Back 4

Located in the right atrium. Right Atrial myocardium. Specialized group of cells called sinoatrial node cells (pacemakers). Electrical signals are passed through gap junctions, intercalated disk and cell to cell contact. Sets the rhythm of the heart. Regulated by autonomic nervous system - including sympathetic and parasympathic (vagus) nerves. Fastest rhythm, intercalated disk is a type of a gap junction in cardiac muscle.

Front 5

Atrioventicular Node (AV)

Back 5

Located at the intersection between the 2 atriums and 2 ventricles. SA node is connected to AV node. Like SA node, collection of cells. Have 2nd fastest rhythm.

Front 6

Action Potential Graph of SA and AV node

Back 6

Never comes to rest. As heart cells beat independently, important in heart transplant (autonomicity)

Front 7

Slope of SA node

Back 7

Can change through the vagus (beats slower). Increasing rate is done by symphatic nervers. This is done by changing permeability of Ca/Na. Parasympthetic makes it harder (decrease slope, Ach is the neruotransmitter). While sympathetic makes it easier (increase slope, Noe is the neurotransmitter)

Front 8

Heart Conditions

Back 8

Bradycardia - lower heart rate

Tachycardia - Increase heart rate

Arrhytmia - heart rate which is irregular

Front 9

Electrical circuit

Back 9

Starts in right atrium in SA nodes goes to AV nodes

Front 10

P Wave

Back 10

Represents atrial depolarization. Time to go and distance from SA to AV node. First wave in ECG. Atriums contract. AV function to lower impulse and rate from SA node to allow the arteries to contract before ventricle. Allows to push all blood to ventricles.

Front 11

Bundle of His (AV Bundle)

Back 11

Connected to AV. Acts as electrical signal between atrium to ventricles. The right bundle branch supply the right ventricle. The left bundle branch supplies the left ventricle (bigger branch). His = axons. Depolarization, contraction starts on inside heart going to outside layer of heart.

Front 12

Purkinje Fibers

Back 12

As branches diverge, they conduct the impulse to purkinje fibers. Which are located between myocardium and endocardium.

Front 13

3 layers of heart

Back 13

Epicardium (external), myocardium (middle layer), endocardium (inner layer)

Front 14

QRS

Back 14

Tells depolarization of ventricles. Larger than P waves. The time that take signal to travel from AV node to myocardium. Blood from atrium to ventricles, blood to rest of the body.

Front 15

ECG vantage points

Back 15

ECG placed at different locations, reads different vantage points. Information coming to you. Up stroke. Away down stroke.

Front 16

Depolarazation

Back 16

Squeezing the muscle from apex to base

Front 17

99% of muscle in ventricle, mask everything in atrium. Left has 3-5 x mass than right ventricle. Left ventricle takes more time to depolaraize than right ventricle.

Front 18

T - Wave

Back 18

The left ventricle depolarizes coming back to rest. Contraction is over

Front 19

Apex

Back 19

Lowest Part of Heart Base

Front 20

Systole

Back 20

Contraction, pushes blood to adjacent chamber

Front 21

Diastole

Back 21

Relaxation, chambers fills with blood. If atrium systole, ventricles must diastole and vice versa. Blood goes from apex to base

Front 22

V- tach

Back 22

Rapid heart beat, improper electrical activity. Contraction not great enough to be bigger than resistance to allow blood flow.

Front 23

Equation of blood flow

Back 23

Q(blood flow)= Change in pressure by ventricles (ventricular contraction) / Change in resistance (by arteries, vascular resistance)

Front 24

Isometric Contraction

Back 24

Increase in tension, no change in length

Front 25

Calcium Plateu

Back 25

Ca ions released from sacroplasmic recticulum allows to cause contraction of muscles. Longer plateau, more contractions. Insure maximum overlap of actin and myosin (strained muscle). Increase Ca plateau to overcome heart failure, increase pressure

Front 26

Refractory Period

Back 26

Two parts. Absolute and Relative. Absolute cannot have another action potential, relative can have action potential following absolute.

Front 27

End Diastolic Volume (EDV)

Back 27

Is the amount of blood in a ventricle at end of a diastole, just before contraction begins. All blood that could be in ventricle, the maximum amount.

Front 28

Preload

Back 28

The degree of stretching in venricular muscle cells during ventricular diastole. It is directly proportional to EDV. It affects the ability of muscle cells to produce tension. As sarcomere length increases past resting length, the amount of force produced during systole increases.

Front 29

Stroke Volume (SV)

Back 29

Is the volume of blood pumped from one ventricle of the heart with each beat, around 70% of edv. SV = EDV -ESV

Front 30

End Systolic Volume (ESV)

Back 30

Is the amount of blood that remains at the end of ventricular systole, at the end of contraction.

Front 31

Cardiac Output

Back 31

The amount of blood pumped by the left ventricle in one minute. Calculated by Heart Rate (HR beats/min) x Stroke Volume (ml/beat)

Front 32

Total Peripheral Resistance (TPR)

Back 32

The resistance of the entire cardiovascular system. For circulation to occur, the circulatory pressure must overcome TPR.

Front 33

Afterload

Back 33

Is the amount of tension that the contracting ventricle must produce to open the semilunar valve (SA) and eject blood

Front 34

Mean Arterial Pressure (MAP)

Back 34

Is the average pressure in arteries during one cardiac cycle. Cardiac Output x TPR = MAP

Front 35

Baroreceptor Reflex

Back 35

Are specialized receptors that modify MAP. They can release NE due to sympathetic nerves. They change blood pressure

Front 36

Nerves and Heart

Back 36

Both parasymphathetic nerves and sympathetic nerves go to heart. Muscarinic receptors respond to Ach in parasympathetic while B1 respond to NE in sympathetic. Both can affect heart rate. While A1 receptors are in blood vessels such as arteries and veins

Front 37

Venous Return

Back 37

Is the amount of blood returning to heart through veins

Front 38

Blood Pressure

Back 38

The pressure exerted by blood against the walls of artiries

Front 39

Heart Attack

Back 39

Using more oxygen than produced, ischemia

Front 40

Frank Starling Law

Back 40

Increase ESV, increases SV

Front 41

Cardiac Failure

Back 41

Fail of contraction of actin and myosin

Front 42

Side Affect

Back 42

Affect Contractility

Front 43

Different between Central and Peripheral Circulation

Back 43

Central - Heart

Peripheral - Everything Else

Front 44

Arteries and Arterioles

Back 44

Both are distributing vessels. Arteries - carry blood away from heart toward a peripheral capillary. Arterioles - the smallest arterial branch. They determine TPR and control blood flow into capillary bed

Front 45

Capillaries and Fenestrated, and continous non fenestrated Capillaries

Back 45

Capillaries - site of gas exchange. Oxygen gets into tissue, Co2 out.

Fenestrated - contain pores that penetrate the endothelial linings, which allow rapid exchanges of water and solutes between blood and tissue fluid.

Continous non fenestrated - do not have pores

Front 46

Veins and venules

Back 46

Store blood, have low pressure thus prevent backflow of blood.

Venules - are smaller version of veins, which supply bllod from capillaries to veins

Front 47

Capillaries are the most numerous. A shock occurs when all capillaries are open, as not enough pressure to push blood. Arterioles and veins have 2nd largest surface area. Greatest pressure drop occurs across arterial network. Right atrium is least pressure. Left ventricle has highest. Blood flows goes slow at greatest surface area thus maximize diffusion in capillaries and arterioles controlling TPR.

Back 47

NA

Front 48

Autonomic Nerves

Back 48

Cannot control cardiac and smooth muscles. Sympathetic - goes to Alpha 1 receptors on all blood vessels and B1 receptors in heart such as Heart Rate. NE is the neurotransmitter

Front 49

Parasympathetic

Back 49

Neurotransmitter Ach. Zero affect on blood vessels. Muscarnic receptors in the SA and AV nodes. Affect the electrical conduction, the rate of heart rate. The Vagus is the main nerve.

Front 50

Poiseuille's Law

Back 50

Pressure comes from ventricles contracting, while resistance comes from blood vessels

Front 51

Q = change in pressure / change in resistance

Back 51

The more pressure needed to generate to overcome resistance, need more muscles to be used, more oxygen is needed. Stroke Work

Front 52

Structure of Heart

Back 52

Four chambers. 2 in top, atrium. 2 in bottom ventricles. Atrium - recieve blood from body. Lowest pressure in Right Atrium 3mm Hg, highest in left ventricle 120 mm Hg. Right ventricle connected to right atrium with tricuspid valve. Ride side gets blood from body to lungs. Right side collect blood from body and pump it to lungs. Called the Pulmonary circuit.

Front 53

Blood comes from lungs through pulmonary veins to the left atrium. Sends blood to left ventricle through bicuspid valve. Called systemic circuit, get oxygenated blood to rest of the body. Hemagoblin in used

Back 53

Ventricles generate pressure, left ventricle has 3-4 more myocaridum mass than right, able to generate more pressure as there is more resistane. Poscille's Law

Front 54

Autonomaticity

Back 54

Cardiac Muscle contraction happens on its own, as can reach threshold independent. Right atrium. SA node cells have fastest rhytehm. Parasympthic slows down working on muscarnic, sysmpthetic faster working on B1 receptors. Autonomic affect the peremebility of NA

Front 55

ECG

Back 55

Electrical Circuit of Heart

Front 56

P - Wave

Back 56

Atriums contracting. Time from SA node to AV node

Front 57

QRS

Back 57

Ventricles contracting AV Node to Hins Purkirje fibers

Front 58

T-Wave

Back 58

Repolization of ventricles left takes more time

Front 59

Systole and Dystole

Back 59

Contraction, Relaxation. Atrium contract 1st, venctricles dystole. And vice verse. Nerves force teamowrk in electrical circuit, no autonomaticity

Front 60

More calcium, more contraction, calcium plateau influx of Ca2+

Back 60

NA

Front 61

Refractory Period . Relative, absloute

Back 61

Measure of time. Relative - can induce 2nd action potential cells are ready. Absloute - cannot generate contraction cells are not ready

Front 62

EDV

Back 62

End Diastole Volume (pre load) amount of blood in ventricles prior to contraction

Front 63

ESV

Back 63

End Systolic Volume, amont of blood left following contraction

Front 64

Stroke Volume

Back 64

EVD-ESV. Amount of blood pumped out

Front 65

Cardiac Output

Back 65

Heart Rate x Stroke Volume. Heart rate is affected by nerves

Front 66

Frank-Starling Principle

Back 66

More EDV, more SV. Too much, over stretching of actin and myosin lead to heart failure.

Front 67

Venous Return

Back 67

The amount of blood returning to the heart through veins. Left Atrium

Front 68

Baroreceptors

Back 68

Sense change in pressure can change outflow of Ne is sys nervous system, affecting venous return and Heart Rate

Front 69

Cardiac Cycle

Back 69

The period between the start of one heart beat to the beginning of the next one

Front 70

Passive Filling

Back 70

Blood comes from the venous system to atrium and then ventricles. Doesn't require any action on heart. AV valves are open. SA valves are closed. Actin and myosin overlap = maximum contraction. Frank-Sterling Law. Atrium in dystole, ventricles in dystole. ECG show nothing. 90% of EDV

Front 71

Rapid Filling

Back 71

SA node is activated atrium contracts (systole) P wave is shown in ECG, while ventricles in dystole. 100% of EDV, actin and myosin overlap is maximized. All EDV is filled in ventricles. AV valve open, SA valves are closed

Front 72

Isovolumetric Contraction

Back 72

Increase tension in myocardium in order to overcome resistance to let blood flow. Still too much resistance. See QRS wave, ventricles depolarize from apex to base, endocardium to the epicardium, inside to outside. No change in length of myocardium. Blood is forced from apex to base to Atriums, AV valves close. Make first sound heart beat, S1. First time all 4 valves close. Ventricles begin to contract/ systole. Atriums dystole. S1=Lubb sound

Front 73

Principal Veins

Back 73

Left side pulmonary veins, right side is superior vena cava, inferior vena cava and coronary sinus

Front 74

When enough pressure exceeds resistance, blood flow occurs. Recruit myocardial cells to generate pressure to open SA valves. 100% EDV, no change no lost in blood

Back 74

NA

Front 75

Rapid Ejection

Back 75

P>R, enough pressure to overcome resistance. Move blood out of ventricles to pulmonary artery in right side, left side is arota. Min volume in arteries, maximum in ventricles. Blood being pushed through tissues. SV x HR = CO. CO - amount of blood leaving ventricles at time. Preload=EDV, Afterload=TPR. SA valves open due to pressure. AV are closed. Forces flow of blood from ventricles to arteries. Volume in Ventricles decrease. EDV max, becomes EDV min = ESV as volume in ventricles as in systole. Volume in vessels is little but increase to maximum in artries. Atriums in dystole

Front 76

Complience

Back 76

Vessels can swell, strectch and come to original phrase.

Front 77

Isovolumetric Relaxation

Back 77

See a T-Wave, ventricles undergo relaxation/dystole. This creates a negative pressure. Blood from veins come back from ventricles. Hear 2nd heart sounds, Dubb Sound S2 which comes from closesure of SA node. All valves close, atriums start to fill with blood.

Front 78

Enough blood in atriums, so pressure exceeds and opens SA valves. Passive fillings starts again as blood moves to ventricles

Back 78

NA

Front 79

Pc- Capillary Pressure

Back 79

Which is the pressure that drives fluid out of the capillary (filtration). Function of Ventricular Pressure

Front 80

P o

Back 80

Osmotic Pressure - Is indication of albumin.

Front 81

Ph

Back 81

Hydorstatic, has to do hemodynamics

Front 82

Pressure

Back 82

Pc - Ph - Po, determines r absorption/filtration

Front 83

In Arterial Network

Back 83

Have greatest pressure drop and greatest surface area. Pc > Ph+po. Filtration occurs. Blood goes slow as enters largest surface area, which lowers the diffusion barriers. Which facilitate diffusion

Front 84

Filtration

Back 84

Is the removal of solutes as a solution flows across a membrane, through endothelial cells, which are spacing. Gasses, fluids and electrolytes pass through fenestrated cells. Which are cells with pores. Forces blood from blood vessels into cells/tissues where tissues is a collection of cells with similar function. Supply needed is oxygen

Front 85

In capillaries and veins network

Back 85

Capillary pressure drops while osmotic and hydrostatic pressure stays the same. Thus re absprtion occurs, reabsorbing what we filter

Front 86

Filtration>Reabsoprtion

Back 86

Generally, so lympth is filtrated but not reabsorbed. Part of the immune system/cancer cells.

Front 87

Edema

Back 87

Swelling Occures when filtration exceeds reabsorption by alot.

Front 88

Sphygmomanometer

Back 88

Used to measure blood pressure. Listen to korohoff's sounds. Stops blood flowing in artieries, release pressure to allow blood to flow again. First Sound is systolic pressure. Dystolic pressure is second sound

Front 89

Caclulations

Back 89

Pulse Pressure (PP) = Systolic - Dystolic

MAP = 1/3(PP) + Dystolic

Pre load - EDV

After load - TPR

Stroke Volume = EDV -ESV

Front 90

Respiratory System

Back 90

Functions

1) Deliver O2 and eliminate Co2

2) Assist in buffering blood pH

Front 91

2 types of ventilation

Back 91

Pulmonary Ventilation - is the amount of air that gets into lungs

Alveolar Ventilation - is the amount of air reaching alveolar surfaces of the alveoli where gas exchange occures

Front 92

Tidal Volume

Back 92

Volume moved into lungs during normal breathing. 500 mL

Front 93

Breath Rate

Back 93

Number of breaths per minute

Front 94

Alveolar Ventilation calculation

Back 94

AV = breathes per minute (F) x (Tidal Volume - Anatomic Dead Space). Where TD is 150 mL.

Front 95

Anatomic Dead Space

Back 95

Volume that is lost from trachea to alveloi sacs

Front 96

Breathing

Back 96

A somatic nerve called the Phrenic (carnial nerve C3,C4,C5) simulates the diaphragm (a skeletal muscle). The diaphragm then contracts, pulls it down increasing volume, decrease pressure and breath in. Vice Versa for exhaling.

Ach is the neurotransmitter reach nictonic receptors in the saclorlema, t-bubules- then sacroplasmic rectilum which releases Ca to bind with troponin and tropmoysin thus contraction

Front 97

Fissure

Back 97

Natural division in body/tissue

Front 98

Alveoli sacs

Back 98

are located in the lungs

Front 99

Lungs move from 6 to 8, 8 to 10, 10 to 12

Back 99

NA

Front 100

Boyle's Law

Back 100

P = 1/v. Increase in volume, decrease in pressure happens in breathing. Increase in pressure, decrease in volume happens in exhaling

Front 101

Breathing/Exhaling

Back 101

Expansion of lungs increase volume, decrease alveloi pressure. So lower than atmospheric pressure, so air flows into lungs, active process. While passive process is exhaling

Front 102

Pleura

Back 102

Is a membrane which surrounds the lungs, it is two layered.

Parietal Pleura - is on rib-cage

Visceral Pleura - is under the lungs.

Front 103

Pleura Pressure

Back 103

Is the pressure formed by water molecules which exists in space between parietal and visceral. It keeps the lungs expanding. As lungs are elastic tissue and they have the tendency to collapse.

Front 104

Every time the bronchi split, the pulomanry artery also splits.

Back 104

1:1 ratio

Front 105

Alveloi are made up of 3 cells

Back 105

Type 1 - endothelial cells, allow diffusion to occur

Type 2- Helps the lung to expand

Macrophage- Immune System

Front 106

Diffusion

Back 106

Occurs at alveloi with capillary beds, due to small membranes, between blood and air. CO2 diffuse into capillaries to be exhaled while O2 is diffused with haemoglobin into capillaries and blood stream

Front 107

Pharynx

Back 107

The throat. Upper respiratory tract. Tubes muscular. Takes air from the nasal and oral cavity to the larynx.

Front 108

Larynx

Back 108

Where voice cords are located. Opening to the upper respiratory system

Front 109

Epiglottis

Back 109

Is a flap that is attached to the entrance of the larynx. It prevents food from going into the trachea and instead directs it to the esophagus. Allows air to get to the larynx.

Front 110

Trachea

Back 110

Is a windpipe, a tough flexible tube below the larynx. Contains 15-20 tracheal cartilages rings

Front 111

Carina

Back 111

Is the area in chest where trachea splits into left and right primary bronchi, which enter the lungs. Where they split into secondary bronchi and into tertiary bronchi over 20 times until reach alveloi sacs

Front 112

Fick's Law

Back 112

Decrease barrier, increase surface area and more difference in concentration for easier diffusion

Front 113

Dalton's Law

Back 113

Calculates partial pressure. Multiply % of gas in atmosphere by 7.60 for amount of % of gas available for diffiusion

Front 114

Endothelial Cells

Back 114

Form linings of blood cells make diffusion possible

Front 115

Spirometer

Back 115

Instrument to measure respiratory performance

Front 116

Tidal Volume (Vt)

Back 116

Amount of air you move into or out of your lungs in single respiratory cycle 500 mL

Front 117

Inspiratory Reserve Volume (IRV)

Back 117

Is the amount of air that you can take in over and above the tidal volume

Front 118

Expiatory Reserve Volume (ERV)

Back 118

Is the amount of air you can voluntarily expel

Front 119

Residual Volume

Back 119

Is the amount of air that remains always in your lungs, never leaves correlated to the anatomic dead space

Front 120

Vital Capacity

Back 120

Is the maximum amount of air that you can move into or out of lungs in single respiratory cycle. Sum of IRV (Inspiratory Reserve Volume)+ERV (Expatory Reserve Volume)+Vt (Tidal Volume)

Front 121

Total Lung Capacity

Back 121

Total volume of your lungs. Calculate it by adding vital capacity and residual volume. Maximum amount of air possible

Front 122

Forced Expiatory Volume in 1 Second FEV1

Back 122

Is the volume that can forcibly be blown out in one second. Significant to calculate lung diseases

Front 123

Pulmonary artries

Back 123

Bring blood into lungs

Front 124

Pulmonary veins

Back 124

Bring blood from lungs to left atrium

Front 125

RBC (erytherocytes)

Back 125

Are important due to hemoglobin (Hb). Alveloi sac high concentration of oxygen, low in CO2. While RBC high in CO2, low in O2. O2 diffuse to blood, CO2 diffuse to alveloi sac. Great concentration difference. Alveloi have lowest diffusion coefficient. 200 x affinity to poison CO2 than oxygen.

Front 126

Oxyhemoglobin

Back 126

HbO2, hemoglobin binds to oxygen molecules after giving Co2

Front 127

Cells and tissue use O2 to produce energy

Back 127

By products which are waste such as Co2 needs to get rid of. 98% of O2 used with hemagoblin, 2% dissolved in plasma

Front 128

Hemogoblin can only carry 50% of Co2. Another 2% of Co2 dissolved in plasma. Major Co2 left over

Back 128

Co2+H2O - carbonic anhdrayse - H2C03 - H +HCO3. The enzyme helps to dissolve left over CO2, only in RBC. HCO3 (bicarbonate) is a major buffer of blood to neutralize acidity.

Front 129

Chloride Shift

Back 129

Exchange of HCo3 bicarbonate with Cl- across RBC, to naturalize acidity 7.4 pH. HCO3 comes into RBC while Cl leaves

Front 130

Oxygen and Hemoglobin

Back 130

Additional oxygen is released by Hb if:

1) pH decreases. As active tissue produce acids which lower pH. Metabolic activity of tissue

2) If temperature increases

3) If greater concentration of 2-3 biphosphoglycrete or BPG in blood

All shift curve down and left of oxygen dissociation

Front 131

O2+C6H12O6+ADP - Co2+H20+ATP in cells

Back 131

Alveloi gets CO2 out of RBC and RBC gets O2 from Alveloi through diffusion.

Front 132

Carbaminohemoglobin

Back 132

CO2 + Hb

Front 133

Pulmonary Stretch

Back 133

Receptors in lung tissue, Hering-Breur Reflex make sure lungs aren't overstretched.

Front 134

Restrictive Lung Disease

Back 134

Are characterized with reduced volumes of the lungs, in other wordsrestrictive lung diseases lower the total lung capacity (TLC)

Front 135

obstructive lung diseases

Back 135

Shortness of breath occurs due to the difficulty of exhaling all thenecessary air from the lungs due to smoking...